Unit 4: Environment and Survival

Topic 5: On the wild side

4.5.1
A particular species can be identified using the features (the
phenotype) which are characteristic to only that species. Species
with similar phenotypes are likely to be related to each other. A key
of characteristics is used to identify the species
Organisms are classified into families according to similarity of
features. The families start of large, but rapidly become smaller.
This is the basis of a hierarchical classification system
Kingdom
Phylum
Class
Order
Family
enus
!pecies
Ta"onomy: the science of classifying liing things.
#iodi$ersity: the ariety of life on our planet, measurable as the
ariety within species, between species, and the ariety of
ecosystems
!f two organisms can interbreed to produce fertile offspring they
are the same species. !f not, they are different species
"inomial System: #eli$ catus !talics in print
(% names) %nderlined in hand
1
SNAB A2 Revision Notes
There are & kingdoms &nimals' Plants' Fungi'
Protoctists' Prokaryotes
(ou need to know the main characteristics o)
each kingdom
enus: tells you what group the
species is from
(has a capital letter)
species: tells you the e$act
species
(small case letter)
'rokaryotes
(icroscopic prokaryotic cells () * &m long rather than +,*+,,m)
-ack of a nucleus (./A in cytoplasm) and possibly plasmids
-ack of membrane*bound organelles
'resence of 0,s ribosomes
/o cytoskeleton
Protoctists
1ukaryotic cell structure
Simple body form, either unicellular, filamentous (chains), colonial (ball) or
macroscopic (large and isible)
The 'roctoctist2s kingdom tends to be full of organisms that do not fit into any
other 3ingdom e.g. algae and yeast
Fungi
4eterotrophic nutrition (get food from eating, unlike plants)
(ade of a network of *yphae, which form a 5. structure called a +ycelium.
(look up (odule + notes)
6all walls containing chitin
Plants
The distinguishing features of the 'lants are7
(ulticellular with eukaryotic structure
6ell walls containing cellulose
6omple$ body form
'hotoautotrophic nutrition (make food themseles through '8S)
'resence of photosynthetic cells with chloroplasts
) stages in the life cycle: a diploid spore*producing stage and a haploid
gamete*producing stage.
&nimals
The distinguishing features of the Animals are7
(ulticellular with eukaryotic cell structure
6ells without cell walls
4eterotrophic nutrition
4ighly organised organs and tissues including nerous co*ordination
The only haploid cells they hae are gametes
2
,istinguishing Characteristics o) the Kingdoms
4.5.%
!ndiiduals in the same species look different (hae different
phenotypes). This is called $ariation
9ariation is caused by7
+. The genotype of the indiidual (i.e. which alleles they hae)
). The enironment
enetic di$ersity describes the range of different genotypes
within a species. !f there are few genotypes the genetic diersity is
small. !f there are lots of genotypes the genetic diersity is large.
6auses of :enetic .iersity:
+. !ndependent Assortment
). (utation
5. ;andom fusion
<. 6rossing Oer
3
&d$antages of little genetic diersity
&d$antages of wide genetic diersity
All indiiduals hae a preferential
phenotype
-ess chance of genetic disease
-ess chance of e$tinction when faced with
disease (i.e. some indiiduals will hae a
phenotype that allows them to surie)
1nironment has less effect on phenotype
Species more likely to surie enironment
change
Species more likely to colonise
Allows access to more niches, therefore
less interspecific competition
/atural selection = speciation can occur
enetic di$ersity
-ndependent &ssortment > which allele of each pair goes into
which gamete. This is caused by the orientation of homologous
pairs of chromosomes during metaphase ) of meiosis
6hanges in the se?uence of bases in codons (mutation) cause
genetic ariation. This usually occurs by ./A being improperly
copied or damaged. 6hemicals (mutagens) and radiation can do
this.
1ach gamete is different. Therefore, by combining different
gametes new ariation occurs (random )usion).
.uring meiosis sections of ./A are swapped between homologous
chromosomes (pairs of chromosomes). This creates more
ariation by creating new combinations of alleles (crossing o$er)
4
,ihy.rid Cross
4.5./
.ihybrid 6rosses are for crosses inoling two different genes
() loci).
A > 'urple stem, a > :reen Stem, . > "ig -eaes, d > little
leaes
5

Parents Phenotype: Purple stem & Purple Stem &
Big Leaves Big Leaves
Parents enotype: !a"# !a"#
ametes:
$1 enotype:
$1 Phenotype: % : 3 : 3 : 1
!&B& : !&'' : aaB& : aa''
Purple & Big : Purple & Little : reen & Big : reen & Little
!#
a"
!" !#
a"
!"
a# a#
!"
!"
!#
!#
a"
a"
a#
a#
! ! " "
! ! " # ! ! # #
! ! " #
! a " " ! a " #
! a " "
! a " #
a a " "
! a " #
! a # #
a a " #
a a # # a a " # ! a # # ! a " #
0cological !ampling Techni1ues
4.5.4
#iotic Factor: A liing ariable within the ecosystem, which affects the surial
of organisms. 1$amples include predation, competition, and pollution from
e$creted waste.
&.iotic Factor: A non*liing ariable within the ecosystem, which affects the
surial of organisms. 1$amples include temperature, light, and water.
2andom !ampling (?uadrats placed at randomly generated interals)
%sed where habitat is uniform
;emoes obserer bias
%sed in a large area
%sed if time is limited
!ystematic !ampling (?uadrats placed at regular interals)
%sed to show 3onation
%sed where there is continuous ariation
%sed to sample linear habitats (e.g. a roadside)
) types of systematic sampling techni?ue7
-ine Transect:
%sed where time is limited
%sed to isually illustrate how species change along a line
"elt Transect:
'roduces more data, gies detail about species abundance down the line
as well as range
Shows species dominance down the line
4hat inter$al should .e used5
Transects can either be continuous with the whole length of the line being
sampled, or samples can be taken at particular points along the line
#or both line and belt transects, the interal at which samples are taken will
depend on the indiidual habitat, as well as on the time and effort which can be
allocated to the surey.
Too great an interal may mean that many species actually present are
not noted, as well as obscuring @onation patterns for lack of obserations.
Too small an interal can make the sampling time consuming, as well as
yielding more data than is needed.
(
4.5.5
An e$ample of a 6amed 0n$ironment
!s the "ritish 2ocky !eashore
&.iotic #actors include7 dessication, salinity, wae action, temperature, water
aailability, substrate, aspect, p4 etc
#iotic #actors include7 interspecific competition, intraspecific competition,
predation, food aailability, presence of e$creted wastes
Species liing in the ;ocky Sea shore
Splash Aone: 7ichen B can surie dessication = temp ariation, re?uires little
nutrient
%pper Shore: #lack Tar 7ichen B can surie long periods without water, grows
slowly, but is less tolerant to dessication than lichen.
(iddle Shore: 0ggwrack B (ore water aailability, less temp range, but more
predation from herbiores and carniores
-ower Shore: Kelp B constant enironment, usually submerged, lower light leels,
intense competition from same and other species
.on2t learn this case study if your teacher gae you notes
on a different habitat. -earn this study if you2re desperate
Adaptations of Species in trophic leels
)
&.iotic Factors hae more
effect going up the beach
#iotic Factors hae more
effect going down the beach
4.5.8
(icro*algae ( #ladderwrack ):
+. 4as bladders of /
)
that allow it to float (to
reach light)
). Tolerates fresh water
5. 4as specialised gonads (resceptacles) which
release lots of sperm into the sea
<. 4as a specialised hold)ast that anchors it to
rocks
&. 4as )uco"anthin pigments that absorb more
light than chlorophyll
(icro*algae -impet .ogwhelk 6rab "lenny Oystercatcher
7impet:
+. 4as a mantle organ that makes the shell
). 4as a radula coered in teeth that grind the
microalgae off the rock
5. 4as gills and breathes through a hole in its
head
<. As the limpet clamps to the rock it grinds its
shell, creating a perfect fit with the rock
&. 4ae no se$ for their +
st
year then change
into males 8 females
,ogwhelk:
+. 4as a adapted radula that bores through
barnacle shells
). 4as a groe in its shell that allows it to
breath whilst boring
5. 9ary in colour across species
<. 4as a ery muscular )oot to stop the effect
of wae action
Common !hore Cra.:
+. 4as antennal glands, which allows it to
osmoregulate (it can cope with arying
salinity)
). 6an bubble air through its gills and
breathe out of water
5. Strong claws for snapping open dogwhelk
shells
<. 6arries eggs to be released in optimum
conditions
#lenny:
+. ;etains water in its gill caity, so can
surie out of water
). 'owerful Caws crush crabs
5. 4as a pair of canine teeth behind main
teeth
<. Doung mature off*shore and then moe
back when mature
Oystercatcher:
+. -ong pointed beak for opening shells and
picking fish out of the water
). 6an shut down the circulation in its legs
to stop them cooling the whole bird
5. 4as natural anti*free@e in its blood to
stop the legs from free@ing
<. !s intelligent and can learn techni?ues for
opening shells
.on2t learn this case study if your teacher gae you notes
on a different habitat. -earn this study if you2re desperate
*
4.5.9
7ight ,ependent !tep o) Photosynthesis
-ight .ependent Step:
+. 6hlorophyll absorbs light (remember chlorophyll is the trap in the
bottom of the photosystem)
%
). 6hlorophyll emits electrons
5. 1lectrons are receied by electron carrier proteins in the thylakoid
membrane (electron transport chain)
<. 1lectron transport chain uses high energy electrons to power the
following conersions7 A.' E 'i AT' and /A.' E 4
E
E
e
*
/A.'4
&. Fater is split (photolysis) to produce replacement electrons for
the photosystems, 4
E
for the reduction of /A.' and O
)
which is
e$creted.
The purpose of the light dependent step is to produce AT' and /A.'4.
AT' proides the energy for conerting 6O
)
into glucose and /A.'4
proides the 4 for glucose.
There are three steps in the 6alin 6ycle7
+. 6arbo$ylation : ;u"' )i"es 6O
)
to form :'. This reaction is
catalysed by the en@yme 2u.isco
1+
4.5.:
2u#P
P
CO
%
&7P
lucose
&,P ; P
6&,P
&TP
6&,P*
&TP &,P ; P

7ight -ndependent !tep o) Photosynthesis
). ;eduction : !n a series of reactions :' reacts with AT' and /A.'4
reduced :' to form :A-' (by reducing :' the /A4'4 itself is
o$idised, reerting to /A.')
5. ;egeneration : Some :A-' is conerted back into ;u"' so the 6alin
6ycle can continue. The rest of :A-' is conerted into glucose in a
series of reactions.
A glucose molecule is generated eery 8 turns of the 6alin 6ycle
11
4.5.<
Thylakoid membrane > location of photosystems = electron transport chain
Stroma > site of 6alin 6ycle = photolysis of water
:rana proide large surface area for absorbtion of light
4.5.1=
6PP > PP ? 2
/'' > /et 'rimary 'roductiity (amount of stored chemical energy the
plant has to use for growth. This is directly proportional to .iomass)
:'' > :ross 'rimary 'roductiity (amount of stored chemical energy the
plant earns through photosynthesis)
; > ;espiration (amount of energy lost through respiration, i.e. heat, lost
as 6O
)
etc)
"est analogy is a salary. :'' is the amount of stored chemical energy the
plant earns through photosynthesis. ; is like income ta$. The plant has to
pay Grespiration ta$H because it can2t photosynthesis at night = not all
parts of the plant are capable of photosynthesis. /'' > disposable
income: what the plant has to spend after paying ta$.
1nergy is lost between trophic leels. 1nergy is lost in the following ways7
in respiration (mostly lost through heat), energy still present in egested
food, through moement, through digestion, energy still present in
e$creted materials etc
12
4.5.11
0nergy in
!unlight
/'' in plant
1nergy in 'rimary 6onsumer
7ost energy
7ost energy
Of the +,,I sunlight energy that reaches plants, J5I is conerted into
/''. 1nergy is lost in the following ways7 reflected light, light of
waelengths not useful to plants, passes through leaes, lost in
respiration, lost as heat etc
0$olution: the idea that one species changes into another oer time
6atural !election: .arwin2s suggestion for the process by which eolution
might occur
0$olution .y 6atural !election (.arwinian 1olution)
+. There is ariation in a species
). (ore indiiduals are born than the enironment can sustain, so
some indiiduals must die.
5. The indiiduals that surie tend to be those that hae alleles
which gie them a selecti$e ad$antage in their enironment (i.e.
they are the best adapted to their enironment, e.g. camouflaged).
These are the GfittestH
<. The fittest surie long enough to reproduce and pass their alleles
onto the ne$t generation.
&. Oer a few generations the fre?uency of GfitH alleles increases and
the fre?uency of GunfitH alleles decreases
K. Soon all 8 most indiiduals hae the GfitH phenotype and the GunfitH
phenotype is eradicated
0. This process continues oer many generations
L. Oer this time new mutations occur, which gie new een better
alleles
M. Oer time the mutations accumulate in the phenotype until the
organism is unable to reproduce (i.e. produce fertile offspring) with
the original organisms. At this point a new species has been
produced (speciation)
13
4.5.1%
This process is speeded up by isolation (see <.&.+<) because this stops the
influ$ of alleles from outside and allows new mutations to accumulate in
the genotype more ?uickly
19<: +althus publishes paper on population growth. (althus noticed that
the human population was e$panding e$ponentially. 4e thought that the
human population would outgrow its resources and that this would lead to
famine and war.
,arwin was influenced by this idea, because he noticed that animal
populations grow e$ponentially and then plateau when they reach the
limits the enironment can sustain (i.e. the population si@e is determined
by the enironment)
1:=< 7amarck publishes a mechanism for eolution based on two laws
-aw +: Organs 8 structures grow if they are used. This means that the
enironment determines the phenotype of an organism
-aw ): 6hanges are passed on to the ne$t generation
So a blacksmith, who uses his muscles all day, will grow bigger muscles.
This worksN "ut, will the bigger muscles be passed onto his childrenO /o,
so -amarck2s theory is easy to falsify.
1:5< ,arwin publishes the Origin of species by means of /atural
Selection. 4e publishes with 4allace who wrote to .arwin to discuss his
own ideas about eolution. They were ery similar to .arwin2s and this
prompted .arwin to publish.
!solation is important for eolution because it decreases the si@e of the
gene pool. This stops new alleles coming in from breeding with original
14
4.5.1/
4.5.14
alleles and speeds the accumulation of new mutations (which is what leads
to speciation)
The different types of isolation.
1olution is a theory, not a fact. (any people beliee that species were
created (creationism). Other people beliee in eolution, but by
mechanisms other than /atural Selection. Dou should respect the opinions
of other people, een if you do not necessarily agree with them.
Primary succession is the first stage of the ecological succession of plant
life from abiotic land with no soil to fully support plant ecosystems (e.g., a
forest). !n primary succession, pioneer plants like mosses and lichen,
start to Pnormali@eP the habitat, creating rudimentary soil from their
dead matter. These pioneer plants create conditions for the start of
plant growth and so more comple$ plants like grasses and shrubs begin to
colonise the area.
Oer time the grass area is colonised by small woody plants, which gie
way to small trees and finally, after a few hundred years, large trees
take oer. The large trees represent the clima" community because
succession stops at this point.
15
+ethod o) isolation ,escription
1cological isolation The species occupy different parts of the
habitat
Temporal isolation The species e$ist in the same area, but
reproduce at different times
"ehaioural isolation The species e$ist in the same area, but do not
respond to each other2s courtship behaiour
'hysical incompatibility Species coe$ist, but there are physical reasons
which stop them from copulating
4ybrid iniability !n some species, hybrids are produces but they
do not surie long enough to breed
4ybrid sterility 4ybrids surie to reproductie age, but cannot
reproduce
4.5.15
4.5.18
A good e$ample of primary succession takes place after a olcano has
erupted. The barren land is first colonised by simple pioneer plants which
pae the way for more comple$ plants, such as hardwood trees by
creating soils and other necessities. %nlike secondary succession, which
refers to succession after an enironmental disaster (such as a forest
fire) primary succession occurs on the geologic timescale, oer thousands
of years
Aoos can play a large role in consering endangered species by7
+. 6onducting research
). ;unning captie breeding programmes
5. ;eintroducing species into the wild
<. 1ducating people
2esearch enables scientists to understand the role of a species in an
ecosystem. "y understanding the niche, food web, reproductie behaiour,
habitat, feeding relationships etc scientists can suggest effectie
methods of consering species.
Capti$e .reeding programmes are used to reintroduce species to the
wild, build up population numbers and maintain genetic diersity. !n a small
population many alleles are lost between generations because an indiidual
only passes on &,I of their alleles. 1.g.
; > ;ed, r > white
1(
4.5.19

Parents Phenotype: ,e# ,e#
Parents enotype: ,r ,r
ametes:
$1 enotype:
$1 Phenotype: % : 3 : 3 : 1
!&B& : !&'' : aaB& : aa''
Purple & Big : Purple & Little : reen & Big : reen & Little
r , r ,
!f the parents only hae ) children and they are both ;ed (;;) then the r
allele has been lost. This is genetic dri)t and is a big cause of the loss of
genetic diersity in an endangered species.
To aoid this stud.ooks are kept (basically, a family tree for the captie
animals) so that only non*related animals are bred with each other. This
decreases the change of genetic drift and also decreases the change of
genetic disease.
Fild animals are often introduced to captie breeding programmes to
aoid these problems
2eintroducing species into the wild has some success, but depends
greatly on the species. As a general rule of thumb, the more adanced the
species the more difficult reintroduction is. This is because animals need
to learn specific behaiours e.g. how to hunt, how to reproduce, how 8
where to find shelter, group behaiours. "reeding animals in captie
enironments that mimic the wild has more success because it allows some
of these behaiours to be learned in captiity. #eeding the animals in the
wild also helps surial rates.
0ducating people is essential to conseration. Often Cust doing something
slightly differently will hae a big impact on consering a species e.g.
building roads with tunnels under them for badgers.
!f you get a ?uestion on this in the e$am you2ll need to think. There are no
set facts to learn.
!f you get a ?uestion on this in the e$am you2ll need to think. There are no
set facts to learn.
1)
4.5.1:
4.5.1<
Unit 4: Environment and Survival
Topic 8: -n)ection' -mmunity @ Forensics
4.8.1
Time of death can be measured using the following factors7
o "ody temperature
o 1$tent of rigor mortis
o -eel of decomposition
o #orensic entomology
"ody temperature:
The rate of cooling depends on the situation the body is found in e.g.
6lothing B slows cooling
1*
SNAB A2 Revision Notes
A body cools following an S*shaped
(sigmoid) cure. The initial plateau at
50Q6 lasts 5, B K, min, then the body
cools ?uickly to ambient temperature.
After )<hrs a body has usually
finished cooling and temperature is no
longer useful.
Temperature is measured using a long
thermometer with a wide range.
Temperature is usually taken rectally
or using an abdominal stab.
#ound in water B speeds cooling
#ound indoors B slows cooling
Air moements B speed cooling
1$tent of rigor mortis:
;igor mortis is the stiffening of Coints and muscles. Small muscles stiffen
first and unstiffen last.
(uscles stiffen because they run out of AT', causing the actin and
myosin muscle fibres to stick permanently to each other. (uscles
unstiffen because the muscle fibres begin to break down.
On page L, of your te$t book is a little more detail about the se?uence of
eents that causes muscles to run out of AT'.
-eel of decomposition:
&utolysis is the break down of body tissues using the body2s own en@ymes
from the digestie system and from lysosomes
After this, bacteria from the gut inade tissues and release more
en@ymes. This tends to happen in anaerobic conditions, which faours the
growth of anaerobic bacteria
1%
Temperature o) .ody !ti))ness o) .ody &ppro" time since death
Farm /ot stiff /o more than 5 hrs
Farm Stiff 5 B Lhrs
6old Stiff L B 5Khrs
6old /ot stiff R 5K B <Lhrs
:reenish discolouration of abdomen (5Khrs)

Spreads across rest of body (5K B 0)hrs)

.iscolouration darkens to reddish green (5K B 0)hrs)

.iscolouration darkens to purple*black (0)hrs)

"ody becomes bloated with gas (one week)

:as is released, body deflates = shrinks (one week E)

Autolysis is increased by mild heat and slowed by intense heat. 4umidity
has a big inolement as well B dry conditions slow autolysis and, in some
cases (e.g. mummies) stop it completely.
The presence of wounds, the clothing the person was wearing and the
combination of gases released during decomposition also hae an effect.
#orensic entomology:
The insects found in a dead body can help identify time of death in 5
ways7
+. !f the temperature of the body has remained relatiely constant
the age of the maggots growing in it can be determined by their
starting length and the temperature of the part of the body they
grew in.
6orpse succession:
e.g. a maggot 5mm long found growing at )LQ6 will be roughly ,.5 days (L
hrs old)
). %sing the life*cycle of the maggot to identify age
5. !f maggots are taken from the body, allowed to grow and the time
taken to pupate is recorded7 it is sometimes possible to work
backwards from the pupation date and work out hold the maggots
must hae been when they were taken from the body. This works
because maggots of different species usually take a fi$ed number
of days to pupate.
2+
4.8.%
The identity of a dead person can be ascertained by7
+. !dentity papers
). #ingerprints
5. .ental records
<. :enetic #ingerprint
-dentity Papers: This is ery obious, think about it.
Fingerprints: The skin on fingers, toes etc is ridged into specific
patterns (arches, tented arches, whorls = loops). Sweat and sebum oil is
left behind from our fingers on the things we touch. %sing aluminium
powder or protein stain (e.g. ninhydrin) fingerprints are reealed.
#ingerprints are uni?ue and can be used to identify people.
,ental 2ecords: 6an be used to identify age and to identify a person
based on their dentist2s record of their teeth. This is usually used when
the body is damaged (e.g. a corpse from a fire)
enetic Fingerprint: %sed because ./A is uni?ue to indiiduals (e$cept
identical twins and clones grown by mad scientists). :enetic fingerprinting
looks for the presence of repeated se?uences of bases in the non*coding
sections of ./A (introns). The repeated se?uences are called satellites
and can be ) B < bases long (+icroAsatellite) or & B ), bases long (+iniA
satellite). The satellites are repeated anything from & B &,, times and
this produces a uni?ue ./A signature.
#ingerprinting process:
+. A sample of ./A is copied using '6;
). Sample is cut using a restriction en@yme
5. Sample is run on an electrophoresis gel, often using a ./A sample
of known length to act as a standardi@ation.
<. A southern blot is taken
21
&. ./A is labeled using a ./A probe specific to the satellite
K. An S*ray is taken to reeal the location of the bands of ./A
The fingerprint is the pattern of bands on the electrophoresis gel.
Assuming the original ./A sample has not been contaminated (by e.g. a
hair from the pathologist) the fingerprint will be e$act.
4.8./
Succession on corpses:
The idea that as each organism or group of organisms feeds on a body, it
changes the body. This change in turn makes the body attractie to
another group of organisms, which changes the body for the ne$t group,
and so on until the body has been reduced to a skeleton. This is a
predictable process, with different groups of organisms occupying the
decomposing body at different times. This techni?ue allows you to tell, by
the age and specific species liing on a corpse, how old the corpse is.
Succession and forensic entomology also show if the body has been
moed.
4.8.4
& typical prokaryote
22
2i.osomes. Same function as eukaryotic cells (protein synthesis),
but are smaller (0,s rather than L,s).
6uclear Bone. The region of the cytoplasm that contains ./A.
There is no nuclear membrane.
,6&. Always circular, and not in chromosome form.
Plasmid. 9ery small circles of ./A, containing non*esential genes.
6an be e$changed between different bacterial cells.
Cell mem.rane. made of phospholipids and proteins, like eukaryotic
membranes.
+esosome. Tightly*folded region of the cell membrane containing all
the proteins re?uired for respiration and photosynthesis.
Cell 4all. .!##1;1/T from plant cell wall. (ade of murein (a
protein). There are two kinds of cell wall, which can be distinguished
by a :ram stain:
A: :ram positie bacteria hae a thick cell wall and stain
purple
": :ram negatie bacteria hae a thin cell wall with an outer
lipid layer and stain pink.
Capsule (or !lime 7ayer). Thick polysaccharide layer outside of the
cell wall. %sed for7
+. Sticking cells together
). As a food resere
5. As protection against desiccation (drying out) and chemicals, and
as protection against phagocytosis (being broken down by a white
blood cell).
23
Flagellum. A rotating tail used for propulsion.
& typical $irus
24
Prokaryotic Cells 0ukaryotic cells
Small cells (T & mm) -arger cells (R +, mm)
Always unicellular Often multicellular
/o nucleus or any membrane*bound
organelles
Always hae nucleus and other
membrane*bound organelles
./A is circular, without proteins
./A is linear and associated with
proteins to form chromatin
;ibosomes are small (0,S) ;ibosomes are large (L,S)
/o cytoskeleton
Always has a cytoskeleton
6ell diision is by binary fission 6ell diision is by mitosis or meiosis
;eproduction is always ase$ual ;eproduction is ase$ual or se$ual
9iruses hae a wide range of different structures. Some iruses are
about +,,nm in diameter, whilst others can range from ), B
5,,,nm.
All iruses hae a protein coat (the capsid), which contains genetic
material. The genetic material is either ./A or ;/A, and can be
single or double*stranded.
The irus genetic material (the iral genome) contains only a few
genes, from about ), in the polio irus to more than ),, in the
herpes irus (human genome contains JL,,,,, genes). The iral
genome codes for the proteins re?uired to manufacture the irus.
The protein capsid is made from identical subunits (called
capsomeres). The capsomeres can be arranged into an icosahedral
shape (e.g. polio = herpes), or a cylindrical shape (e.g. T(9 =
rabies) or a loose containment structure (e.g. measles =
influen@a).
!n addition, some iruses also hae an outer membrane enelope, which
allows the irus to penetrate the host cell membrane by
endocytosis. !nfluen@a, 4!9 and measles irus all hae membrane
enelopes.
9iral .amage B Fhat do 9iruses actually do to usO
25
CligandsD
-ike bacteria, iruses hae protein ligands on their capsid that
attach to ligand receptors on eukaryotic cells. After a irus ligand
attaches to a host cell ligand receptor it becomes anchored to the
host cell. The irus attempts to get its iral genome into the host
cell, usually through endocytosis using its lipid membrane. 9iruses
without lipid membranes may hae specialised proteins designed to
help inCect the iral genome into the cell cytoplasm.
(i) 9irus ;/A enters host cell
(ii) 9irus may also inCect ;/A 'olymerase into host cell as well.
(iii) 9iral ;/A and ;/A 'olymerase enter host cell nucleus ia
nuclear pores
(i) 9iral ;/A is copied in nucleus
() 9iral ;/A is transcribed using iral ;/A 'olymerase
(i) 9iral m;/A is translated in the cytoplasm
(ii) /ew 9irus proteins formed
(iii) 9iral proteins associate with copied ;/A forming new
complete iruses
(i$) /ew iruses leae host cell to infect other cells
9iruses that hae a ./A code instead of an ;/A code often insert
their iral ./A into the host cell2s ./A. Other ;/A iruses inCect
the en@yme ;eerse Transcriptase, which makes a c./A copy of
the iral ;/A. The c./A copy is then inserted into the host cell2s
./A. Other iruses (e.g. 4!9) also inCect the en@yme integrase,
which helps insert the iral c./A into the host2s ./A
"e sure you can recall what the 5 iral en@ymes do7
./A 'olymerase:
;/A Transcriptase:
!ntegrase:
Some iruses target specific tissues (e.g. 'oliomyelitis irus targets
motor neurones, 4!9 targets helper T cells, !nfluen@a targets
epithelial cells = rabies irus targets specific brain cells). !f lots of
new irus is being made, these host cell may lyse (burst) and die.
2(
4.8.5 @ 4.8.8
6ourse of infection for Tu.erculosis :
Tu.erculosis (T") is caused by the (ycobacterium tubercolusis
bacterium.
+. (ycobacterium tuberculosis is inhaled into the lungs in
droplets of water = mucus from another person2s lung (droplet
in)ection)
). T" begins to reproduce in the lungs.
5. The bacteria produce to$ins, which damage lung tissue =
cause coughing, increasing the transmission of the disease.
<. The body launches an immune response to the T" bacterium.
&. 4istamine release and inflammation occur (see <.K.0)
K. +acrophages enter the lungs in large numbers.
0. The macrophages engulf the T" bacteria in large groups,
forming a mass of tissue called a granuloma. The inside of the
granuloma is stared of o$ygen, which kills the bacteria.
L. Once the bacteria are dead, the lung heals
#ET
M. T" bacteria can surie inside macrophages as the cell wall of
the bacterium is ery thick and wa$y and is resistant to the
macrophage en@ymes.
+,.The bacterium can surie and reproduce inside the
macrophage for many years without causing infection. Fhen
the immune system is weakened (by stress, malnutrition, or
another disease B 4!9 is a common cause) the T" bacterium
breaks out and re*infects the body.
++. The bacteria reproduce too rapidly for the body to destroy
+). The lungs are progressiely damaged, which eentually leads
to death.
+5.T" can also spread to the lymph nodes in the body, where it
reproduces causing the disease scro)ula
6ourse of infection for Tu.erculosis :
2)
*-F is the 4uman immunodeficiency 9irus, which eentually leads to
Ac?uired !mmunodeficiency Syndrome (&-,!)
4!9 is spread by direct contact i.e. through se$ual intercourse,
blood*to blood transfer (tattoos, needle sharing, piercing = cut*to*
cut transfer).
Once inside the bloodstream an 4!9 infection occurs in 5 distinct
phases7
+. The acute phase. 4!9 irus has a ligand (:'+),), which
attaches to a receptor (6.<) on the membrane of a type of
white blood cell called a *elper T cell. 4!9 rapidly infects
4elper T cells and the irus population increases ?uickly. At
the same time the population of 4elper T cells falls rapidly.
The acute phase ends when the 3iller T cells begin to
recognise infected 4elper T cells and kill them, which slows
the replication of the irus.
). The chronic phase. This can last for many years. The irus
continues to replicate, but the 3iller T cells keep the numbers
in check. 4oweer, because the immune system is weakened
other bacteria and iruses are more likely to infect the
person (T" may reactiate at this point)
5. The disease phase. As the numbers of irus increase and the
numbers of 4elper T cell fall the immune system becomes
weaker and weaker. 1entually a second pathogen will infect
the person (an opportunistic in)ection) which cannot be
fought off. The person will die ?uickly from the secondary
infection and this is the A!.S disease state.
The huge problem with 4!9 is that it mutates ery ?uickly. Once
inside the body the iral antigens change and the (already
damaged ) immune system can2t keep pace with the changes.
Another problem is that 4!9 attacks 4elper T cells, which are
crucial for actiating the " cells and also play a role in actiating
2*
3iller T cells. Fith low numbers of 4elper T cell, the immune system
cannot communicate effectiely and this increases the ability of
4!9 to surie in the body.
4.8.9
/on*specific immune responses:
-n)lammation: damaged white blood cells and mast cells release
histamine at the site of infection. 4istamine causes local arterioles
to asodilate, increasing the blood supply to the area. !t also causes
holes to open between endothelial cells in capillary walls. This causes
local oedema (the swelling associated with inflammation). !t allows
monocytes and neutrophils into the infected area, which engulf and
destroy foreign bodies and pathogens. 1entually phagocytes arrie
and complete the Cob. .ead monocytes and pathogen form pus.
7yso3yme: an en@yme that breaks down bacterial cell walls, causing
them to lyse and die. -yso@yme is made in lysosomes inside
phagoctyes and is responsible for digesting engulfed bacteria.
-yso@yme is also made by the skin, epithelial cells, and is present in
tears
-nter)eron: a protein made by irus*infected cells. !t blocks ;/A
synthesis and therefore stops irus replication
Phagocytosis: the process in which a pathogen is engulfed and
destroyed. (acrophages engulf pathogens using pseudopodia (Gfake
feetH). The bacterium is taken into the macrophage by endocytosis
and enters the macrophage inside a acuole. -ysosomes containing
lyso@yme fuse with the acuole and digest the bacterium inside.
2%
4.8.:
Pathogens hae proteins on their surface that our immune system
has learned to recognise as foreign. These proteins are called
antigens. T cells, " cells = (acrophages all hae the ability to
recognise an antigen and once this has happened, they will trigger an
immune response.
!n addition to this, macrophages hae the ability to present foreign
antigens to T and " cells. Once a pathogen has been engulfed and
destroyed +*C proteins inside the (acrophage stick to the
pathogenic antigen. They are then incorporated into the cell
membrane of the (acrophage, so it can present the foreign antigen
and actiate the T and " cells responses.
Antibodies (also called -mmunoglo.ulins) are proteins produced by "
cellls. They are found in blood plasma, lymph, tissue fluid, tears,
mucus and milk.
3+
!ntigen-'in#ing site
1ach " cell produces a different immunoglobulin molecule which
recognises and binds to a specific antigen. There are oer a million
different " cells in your body, therefore you hae the ability to
recognise and react to a million different antigens.
The $aria.le region of the immunoglobulin protein is what
recognises = binds to the antigen. 1ach ariable region is different,
hence the name.
There are & different families of immunoglobulin molecule in the
human body (:, (, A, . = 1. !g: * also known as *globulin). The
families can be distinguished from each other by slight differences
in the constant region of the protein
1ach antobody molecule contains two pairs of proteins7
* Two heay chains
* Two light chains
1ach pair of chains is held together by disulphide bridges (hydrogen
bonds would be too weak).
1ach immunoglobulin molecule has ) antigen binding sites and can,
therefore, bind ) antigens at one time. This means that a single
antibody molecule can bind to ) pathogens at the same time, which
31
.onstant
,egion
/aria'le
,egion
"isulph#e
Bri#ges
causes pathogens to clump together and form the &nti.odyA&ntigen
Comple".
The formation of the Antibody*Antigen 6omple$ is important
because it7
* !solates pathogens so they cannot infect other host cells
* (akes it easier for macrophages to engulf = destroy the
pathogens.
* Stops the pathogen from entering a host cell
* (akes it easier for T cell actiation as more antigens are
presented in one area
4.8.<
There are two different types of !mmune ;esponse7
A 6ell*mediated !mmune ;esponse
" Antibody*mediated !mmune ;esponse.
/": !solated iruses do not present antigens and therefore
do not trigger either the 6ell* or Antibody*mediated
immune ;esponse. 4oweer, when iruses inade host
cells, iral proteins are e$pressed which become
32
Antibody
'athogen
Antigen
incorporated into the host cell surface membrane ia
(46. These proteins are recognised as antigens.
CellA+ediated -mmune 2esponse:
+. 6ompetent T 6ells recognise a specific foreign antigen using its T
cell receptor.
). Actiated T 6ell undergoes rapid mitosis forming a large number
of identical clone T
5. 6loned T 6ells differentiate into Killer' *elper' +emory or
!uppressor T 6ells.
<. 3iller and 4elper 6ells migrate to the site of infection
Killer T Cells: attach to the infected 8 foreign cell and release the
en@yme Per)orin, which makes holes in the pathogen2s cell membrane
causing it to die
*elper T Cells: stimulate " cells to start producing antibody and
attract macrophages to the site of infection
+emory T Cells: remain in the lymph nodes. They will respond
rapidly if the same pathogen inades the body again, because they
hae the right T cell receptor to recognise the pathogen. This
means that the body can mount an immune response before
infection becomes serious
!uppresor T Cells: stop the immune reaction after about a week
&nti.odyAmediated -mmune 2esponse:
+. " cells are recognise a specific foreign antigen using the
antibody molecules on their surface. " cells can also be actiated
by macrophages = 4elper T cells. Fhen a macrophage digests a
pathogenic cell antigens from the cell membrane get stuck in the
33
macrophage2s membrane7 any " 6ells which come into contact
with the antigen will then be actiated
). The actiated " cell undergoes rapid mitosis and lots of clone "
cells are produced
5. 6loned " 6ells differentiate into either Plasma or +emory cells
4.8.1=
/egatie feedback systems aim to keep something (e.g. blood
UglucoseV or body temperature) at a constant leel.
/egatie feedback works as follows7
+. Signal causes action
). Action has effect
5. 1ffect remoes original
1.g.
+. 4igh UglucoseV in blood causes insulin release
). insulin stimulates lier to take up glucose = conert it into
glycogen stores
34
Plasma Cells
a) 'lasma cells antibody, which is
specific for one antigen only
b) Antibody is transported ia the
lymph to the site of infection
c) Antibody attaches to the specific
antigen
d) An antigenAanti.ody comple" is
formed
+emory Cells
(emory 6ells continue to secrete
antibody for many years, so that if
the body is infected by the same
pathogen the (emory " cells can
produce an instant supply of antibody
before the infection becomes serious
5. UglucoseV falls
4.8.11
*omeostasis is the maintenance of the body2s internal enironment.
This is carefully controlled by a series of systems, which aim to
keep conditions at a stable controlled leel.
"ody Temperature:
"ody temperature is carefully regulated to maintain a steady
50.&Q6, which is the optimum temperature for human en@ymes.
Sensors (thermoreceptors) in the hypothalamus continually monitor
blood temperature and actiate warming 8 cooling processes to keep
the temperature as stable as possible.
35
"ody temperature is normal
1$ercise
"ody temperature rises
.etected by thermoreceptors in hypothalamus
4air erector muscles
cause body hairs to lie
flat
'eripheral arterioles
asodilate
Sweat glands release
sweat onto skin
(ore heat radiated
away from skin
Sweat eaporates
carrying heat away
Tuberculosis bacterium ((ycobacterium tuberculosis) causes )e$er.
4ow does feer workO
All white blood cells communicate with each other and the rest of
the immune system using a class of hormones called cytokines. The
cytokines hae hundreds of different roles and many more are yet
to be discoered. One class of cytokine is the hormone interleukin,
which causes feer.
#eer can be induced by many factors. The general class of
hormones that lead to feer are called pyrogens (interleukin is a
natural pyrogen). 4oweer, bacterial to$ins, iral proteins and
substances produced by necrotic tissue may also trigger feer.
'yrogens trael in the blood to the hypothalamus in the brain. They
bind to receptors there and trigger a comple$ set of reactions that
lead to the production of ':1) hormone, which eleates the
thermoregulatory set point, i.e. it re*sets the body2s natural
thermostat to a higher temperature.
The hypothalamus now thinks body temperature is too low and
triggers a system of responses which aim to generate heat
(thermogenesis) and raise body temperature. These mechanisms
include7 shiering, increased muscle tone, asoconstriction and the
production of thyro$ine hormone (which makes respiration less
efficient, therefore producing more heat).
4.8.1%
3(
-ess insulating air
trapped ne$t to skin
"ody temperature returns to normal
"arrier (echanisms include7
Skin
Stomach Acid
/ormal #lora
1pithelial cells
Skin Adaptations for defence:
The skin is made from ) layers7
* Outer epidermis layer
* !nner dermis layer
The epidermis proides a physical barrier to inading pathogens.
There are ) layers in the epidermis7
A Outer cornified layer, composed of compacted dead dry
cells filled with indigestible keratin protein (which also
forms nails and hair)
3)
" !nner (alpighian layer, site of rapid mitosis and
keratinisation.
The skin also has chemical defence mechanisms7
* sweat = sebaceous glands secrete se.um, which is an oil
with p4 5 B &. This makes the skin acidic
* sebaceous glands also secrete the en@yme lyso3yme, which
is a natural antibiotic. -yso@yme destroys bacterial cell
walls.
Stomach Acid:
!s made from 46l at p4 + B ). it is a ery effectie barrier.
/ormal #lora:
The skin, respiratory tract and gut are coered with commensual
bacteria, which are part of the normal )lora of the body.
6ommensual bacteria are adapted to lie the enironment of the
skin and the gut and the and compete with inading pathogens for
the limited supply of nutrients.
1pithelial cell Adaptations for defence:
+. 1pithelial cells are closely packed = connected by tight
Cunctions forming a continuous impermeable layer
). 1pithelial cells hae cilia, which form a direct physical barrier
preenting pathogen attachment
5. 6ilia Wbeat2 in waes, which helps clear bacteria out of the
lungs and into the throat, where they are swallowed. !ngested
bacteria are ?uickly killed by the low stomach p4 and
digestie proteases. 6ilia also beat in the :! tract.
3*
<. 1pithelial cells secrete mucus, which is trapped by cilia. (ucus
also directly preents pathogen attachment
&. (ucus contains lyso@yme
4.8.1/
"oth T and " 6ells differentiate into (emory 6ells, which remain in
our lymph nodes and wait until we are re*e$posed to the same
pathogen.
Fhen the (emory " cell is actiated by the old antigen it makes
large ?uantities on antibody ?uickly and kills the pathogen .e)ore it
can in)ect us properly. The memory cells proide acti$e immunity.
Fhen we are e$posed to a new antigen it takes us about a week to
be able to make new antibody. 4oweer, a second e$posure to
antigen produces a much faster response, and seeral orders of
magnitude higher leels of antibody are produced.
3%
Antibody made by
memory " cells
proides actie
immunity
'lasma " cells make
lots of antibody on
re*e$posure
Fithout immunity the
leel of antibody
produced by plasma
cells is much less
Passi$e -mmunity is immunity to a pathogen without (emory cells.
!t can occur through antibody inCection or from drinking breast milk
(breast milk contains high UantibodyV)
Actie /atural !mmunity B the process aboe
'assie /atural !mmunity B beastfeeding (antibody in milk)
Artificial Actie !mmunity * accination
Artificial 'assie !mmunity B antibody inCection
4.8.14
Fe hae eoled a ery effectie immune system, consisting of
barriers, non*speficif defence mechanisms and specific ones. !f
we2re so good at fighting infections, why do we still get illO
Answer: pathogens are eoling as well.
So how has T" eoled to beat usO
+. !t is spread by droplet infection, which is the most effectie
method of infection
). !t specifically targets epithelial cells, which means that, when
inhaled, it is e$actly where it wants to be
5. !t does not kill immediately. This means that it has a large window
of opportunity to spread to others
<. !t has a ery thick wa$y cell wall, which means it is partially
protected against lyso@yme
&. !t can surie inside macrophages and lie dormant until the immune
system is weakened, when it can re*infect.
4+
So how has 4!9 eoled to beat usO
+. !t weakens the immune system to increase its chance of surial
). !t stays in the body for years, so it can spread
5. !t specifically targets 4elper T cells
<. !t is spread by se$ual contact, so it is easily spread
4.8.15
Antibiotics work by targeting prokaryotic features not found in
eukaryotic cells, e.g. penicillin targets the cell wall and breaks it
down. 'enicillin can be taken in large doses by humans because it has
no effect on our cells (we hae no cell walls).
#acteriostatic antibiotics stop bacteria reproducing, they do not
kill bacteria
#acteriocidal antibiotics kill bacteria
4.8.18
The effectieness of antibiotics can be measured using a disc
diffusion techni?ue.
+. A .acterial lawn is grown on an agar plate (either by
spreading the bacteria oer the plate, or by using a pour
plate).

). A disc of blotting paper is soaked in antibiotic of known
concentration and placed in the centre of the plate.
41
5. A clear circle of dead bacteria will form around the disc
<. The diameter 8 radius of the circle of dead bacteria is
proportional to the effectieness of the antibiotic
&. This can be compared to other antibiotics, as long as the
same concentration of antibiotic is used. !n addition, one
can also compare the effectieness of an antibiotic with a
disinfectant or sanitiser (e.g. 'henol coefficient)
4.8.19
"acteria are becoming resistant to antibiotics. "acteria deelop
resistance through mutation. A bacteria can mutate and deelop
resistance by7
+. 4aing an en@yme that breaks the antibiotic down
). 4aing a protein which pumps antibiotic out of the cell
5. (utating the structure of the bacterium so that the
antibiotic no longer works
This problem is ery serious. "acteria become resistant because7
+. "acteria mutate ery easily. One in eery million bacteria contains a
mutation. That might sound like a small amount, but consider that
one 1 coli bacterium can reproduce to form a colony of ) million
bacteria in two hours. Oer weeks, months and years that2s a lot of
mutations, some of which will be beneficial
). "acteria reproduce ery ?uickly (they diide eery ),min) so a
bacterium with a beneficial mutation will spread ?uickly
42
5. "acteria hae the ability to pass copies of plasmids from one to
another (conGugation). So a mutation in one bacterium can ?uickly
be copied to others, een others in different species.
<. The use of antibiotics speeds the rise of immunity. !f a bacterial
population is continually e$posed to antibiotic all bacteria will die.
As soon as a bacterium mutates the rest of the bacteria will be
killed off by the latest dose of antibiotic7 now the field is open for
the mutated bacterium to grow without competition.
&. 4umans hae been reckless with use of antibiotics. They are often
gien to people who don2t need them (i.e. they hae iral infections)
or to people who don2t bother to complete the course of antibiotic.
4.8.1:
The eolutionary arms race between bacteria and drug deelopers
is, at the moment, tipped against humans. There are oer +,,
different types of antibiotic and in the <,years since their
deelopment < species of bacterium hae deeloped resistance
against all o) them. 1.g. (ethicillin ;esistant Staphyloccus Aureus
((;SA) has been named the Superbug, because we hae do drugs
left that can kill it.
%nless drug deelopers discoer another branch of antibiotics we2re
not currently using (i.e. another way of targeting prokaryotic
structures without damaging eukaryotic ones) there may well be a
global pandemic of resistant bacteria.
Unit 5: Energy, Exercise and
Coordination
Topic 9: 2un )or your li)e
43
SNAB A2 Revision Notes
5.9.1
6artilage: a tissue made from collagen, which protects bone ends
A muscle: an organ that produces moement by contraction
A Coint: the Cunction between two bones
A tendon: Coins muscle to bone
A ligament: Coins bone to bone to stabilise a Coint
(uscles work in pairs. One muscle produces the opposite moement
from the other muscle, therefore, the pairs are called antagonistic
pairs.
(uscles which cause a Coint to e$tend are called e"tensors, muscles
which cause a limb to retract are called )le"ors.
5.9.%
(uscles are made from muscle fibres arranged into bundles. 1ach
fibre is made from bundles of myo)i.rils, which are e$tremely long,
cylindrical muscle cells.
44
6artilage
Tendon
"one
-igament
(uscle
Synoial #luid
Synoial membrane
A Synoial Xoint
(uscle cells ((yofibrils) Arrangement of myofibrils into a muscle fibre
The functional unit of contraction is the sarcomere. (uscle cells
contain many sarcomeres arranged in parallel. The muscle cell takes
on a characteristic banded appearance because of the regular
arrangement of the sarcomeres. This is called striation.
45
(uscle #ibre
A sacromere. /ote the striated
appearance of the muscle
The sarcomere contains oerlapping
actin and myosin. The myosin is often
called the thick )ilament because the
myosin heads make it appear thick.
The actin is, therefore, the thin
)ilament
+. A nere impulse arries at the
neuromuscular Gunction
). The muscle cell is depolarised
5. 6a
)E
is released from the
sarcoplasmic reticulum inside
muscle cells
<. 6a
)E
bids to Troponin protein in the
thin filament.
&. Troponin protein and Tropomyosin
protein moe position in the thin
filament
K. (yosin binding sites are e$posed
on the thin filament
0. (yosin heads of the thick filament
stick to actin
L. AT' (already bound to the myosin
head) is hydrolysed causing the
myosin head to piot forwards in
the powerstroke
M. As the head piots the thick
filament moes across the thin
filament B muscle contraction
occurs
+,. A.' diffuses away from the
myosin head leaing the AT'*
binding site empty
++. /ew AT' binds = the myosin head
= causes the myosin head to
detach from the actin.
+). The myosin head re*cocks
+5. The head rebinds further up the
myosin.
+<. ;epeat stages 0 to +5 until the
U6a
)E
V falls too low, when
contraction stops
The process by which the thin filaments are pulled in towards each other by
the myosin is called crossA.ridge cycling. !t is how muscles contract.
CrossA#ridge Cycling:
&denosine TriPhosphate (AT') is made from three components7
* ;ibose (the same sugar that forms the basis of ./A).
* A base (a group consisting of linked rings of carbon and
nitrogen atoms)7 in this case the base is adenine.
4(
Key Point: AT' is re?uired to release myosin
from actin. !f AT' leels drop (assuming 6a
)E
is
present) the myosin stays attached to the
actin and the muscle stays permanently
contracted. This is what causes rigor mortis
5.9./
&denine .ase
2i.ose / " phosphate
* %p to 5 phosphate groups. These phosphates are the key
to the actiity of AT'
The energy used in all cellular reactions comes from AT'. "y
breaking the 5
rd
phosphate from the AT' molecule energy is
released, which can be used to power intracellular reactions. The
AT' is then regenerated by recombining the phosphate and A.' in
respiration (or another process e.g. photosynthesis).
The recycling of AT' is crucial for life. #or e$ample a runner uses
JL<kg of AT' in a marathon (more than their total body weight),
yet there are only &,g of AT' in the entire bodyN This means each
that each molecule of AT' has been recycled +K0K times during the
raceN
4ow the energy in AT' is liberated:
4)
Adenosine
AT' > one adenosine
molecule with 5
phosphate groups
attached
01nergy ri2h 'on#3
43+5(678mol9
01nergy ri2h 'on#3
43+5(678mol9
Less energy ri2h 'on#
4135*678mol9
AT' E 4
)
O A.' E '
i

A.' E 4
)
O A(' E '
i

A(' E 4
)
O Adenosine E '
i
Adenosine
1nergy
P
P
/ormally, as soon as AT' has been conerted into A.' E '
i
it is conerted back into AT' using energy from
respiration. 4oweer, during e$ercise A.' may be
conerted into A(' or een Adenosine to proide energy.
2espiration: a process in which the chemical bond energy in
glucose molecules is used to conert 5L A.' molecules into 5L
AT' molecules. O$ygen is re?uired and 6arbon .io$ide and
Fater are produced as waste products.
;espiration occurs in < distinct steps7
4*
Adenosine
Adenosine
1nergy
1nergy
P
2espiration

4%
lucose
lyceraldehyde
Phosphate
lyceraldehyde
Phosphate
2espiration: !tep 1 A lycolysis
)AT's are re?uired

)AT's are made (< oerall)
+ /A.4 is made () oerall)
5.9.4
!tep 2eactants Products !ummary
+.
:lycolysis
(cytoplasm)
+ $ :lucose
) $ AT'
) $ 'yruate
< $ AT'
) $ /A.4
A K6 glucose molecule is split
into two 56 pyruate molecules.
Some AT' is used to split the
glucose molecule in the first part
of glycolysis
).
-ink ;eaction
(mitochondria
matri$)
+ $ 'yruate
+ $ 6oA
+ $ Acetyl 6oA
+ $ 6O
)
+ $ /A.4
56 'yruate is split into a )6
molecule, which is attached to a
6oA en@yme to form Acetyl 6oA.
The remaining carbon atom is
used to form 6O
)
5.
3rebs2 6ycle
(mitochondria
matri$)
+ $ Acetyl 6oA + $ 6oA
+ $ AT'
) $ 6O
)
5 $ /A.4
+ $ #A.4
)
6oA en@yme gies its )6 atoms
to a <6 molecule to form a
temporary K6 molecule. !n a
series of steps the K6 molecule
releases the two 6 atoms as 6O
)

eentually re*forming the
starting <6 compound. The cycle
is then ready to repeat itself. As
the cycle turns AT', /A.4 =
#A.4
)
are formed
<.
O$idatie
'hosphorylation
(mitochondria
christae)
+, $ /A.4
) $ #A.4
)

K $ O
)
5< $ AT'
K $ 4
)
O
The electron transport chain
uses the /A.4 and #A.4
)
made
in preious steps to make lots of
AT'
!n lycolysis a :lucose molecule (K6) is split into ) molecules
of :lyceraldehyde 'hosphate (56). )AT's are re?uired for
this to happen.
Then, each 56 :lyceraldehyde 'hosphate molecule is conerted
into a 56 'yruate molecule. !n the process of conerting one
:lyceraldehyde 'hosphate to one 'yruate, enough energy is
released to conert one /A. molecules into one /A.4
molecules and also to make two AT' molecules.
Oerall7 <AT' are made, )/A.4 are made and )AT's are used.
6et gain: %&TP and %6&,*
5+
Pyru$ate Pyru$ate
:lycolysis takes place in the cytoplasm of a cell
'yruate -actate
!n the lier the lactate is conerted back into pyruate. This re?uires
o$ygen, which is the basis of the GO$ygen .ebtH
!n the 7ink 2eaction a 'yruate molecule (56) is split into a )6
molecule and a 6O
)
. The )6 molecule is attached to a 6oA
en@yme, forming Acteyl 6oA.
;emember, two molecules of 'yruate were made at the end of
:lycolysis, therefore the -ink ;eaction happens twice.
Oerall7 )/A.4 and ) 6O
)
are made.
6et gain: %6&,*
51
!n anaero.ic conditions U4
E
V rises in the mitochondria as there are no aailable o$ygen
molecules to mop it up with and form water. This leads to saturation of the electron
transport chain and a build*up of /A.4 and #A.4). This means U/A.V falls, which stops
the 3rebs2 6ycle. Acetyl 6oA leels build*up, U6oAV falls and the -ink ;eaction stops.
'yruate leels start to riseY
(uscle cells turn pyruate into lactate to stop rising UpyruateV from stopping :lycolysis
(remember, en@yme controlled reactions are reersible and depend on UreactantsV and
UproductsV).
2espiration: !tep % ? 7ink 2eaction
+ /A.4 is made () oerall)
+ 6O
)
is made () oerall)
-ink ;eaction takes place in the matri" of the mitochondria
Pyru$ate
Co& en3yme &cetyl Co&
/A.4 /A.
!n the Kre.sH Cycle the Acetyl 6oA gies its )6 atoms to a <6
molecule (O$aloacetate) forming an unstable K6 molecule
(6itric Acid). The K6 molecule breaks down into a <6 compound
(Succinyl B 6oA) releasing enough energy to make one /A.4.
The two spare 6 atoms are released as two 6O
)
molecules.
Succinyl B 6oA is conerted back into O$aloacetate and this
releases enough energy to make one /A.4, one #A.4
)
and one
AT'. The O$aloacetate can then be used in the cycle again.
;emember, two molecules of Acetyl 6oA were made at the end
of the -ink ;eaction, therefore the 3rebs2 6ycle happens twice.
Oerall7 </A.4, )#A.4
)
, )6O
)
and )AT' are made.
52
2espiration: !tep / ? Kre.sH Cycle
3rebs2 6ycle takes place in the matri" of the mitochondria
) /A.4 are made (< oerall)
+ AT' is made () oerall)
+ #A.4
)
is made () oerall)
) 6O
)
are made (< oerall)
Co& en3yme
5.9.5
O$idatie 'hosphorylation uses the /A.4 and #A.4
)
produced in the preious steps of respiration to make AT'.
1ach /A.4 makes 5AT' and each #A.4
)
makes ) AT'.
4ydrogen atoms from the /A.4 and the reduced #A.4
)
are
passed onto ) the first ) en@ymes of the 0lectron Transport
Chain. These en@ymes are *ydrogen Carriers and they accept
the 4 atoms from the /A.4 and the #A.4
)
.
1lectrons, which made up the chemical bond between the
hydrogen atoms and the /A.4 8 #A.4
)
are passed onto 5
0lectron Carrier en@ymes further down the 1lectron
Transport 6hain.
53
#A.4
)
AT' #A.4
4
)
O
/A.
/A.4
AT'
AT'
Z O
)
E )4
E
AT'
A.' A.'
2espiration: !tep 4 ? O"idati$e Phosphorylation
O$idatie 'hosphorylation takes place using en@ymes embedded in
the inner membrane of cristae of the mitochondria
4
E
6arrier 4
E
6arrier e
*
6arrier e
*
6arrier e
*
6arrier
)e
*

5.9.8
At the end of the 1lectron Transport 6hain, the electrons are
recombined with the 4
E
atoms and o$ygen, to form water. This
is the only, but crucial, part of respiration to inole o$ygen.
/A.4 starts at the first 4ydrogen 6arrier and has enough
energy to phosphorylate 5A.'. #A.4
)
has less energy and
starts at the second 4ydrogen 6arrier, it generates ) AT's
4here does the /: &TP come )rom5
:lycolysis produces7 )AT' )/A.4
-ink ;eaction produces7 )/A.4
3reb2s 6ycle produces7 )AT' K/A.4 ) #A.4
)

Total < AT' +,/A.4 ) #A.4
)

1ach /A.4 produces 5AT' total production is 5,AT' from
/A.4
1ach #A.4
)
produces )AT' total production is <AT' from
#A.4
)
:rand Total <AT' E 5,AT' E <AT' > /:&TP
54
Chemiosmosis of 4
E
ions
from the mitochondrial
enelope into the matri$
through AT' Synthetase
proteins is what actually
generates the AT' in
respiration
The electron transport chain uses the process of chemiosmosis
(the diffusion of ions across a membrane). 4
E
ions are actiely
pumped into the mitochondrial enelope. This is done by the
proteins in the electron transport chain, using the energy
stored in /A.4 and #A.4
)
.
The U4
E
V builds up to ery high leels in the enelope. 4oweer,
4
E
cannot escape because it is charged (hydrophilic) and
therefore cannot moe through the phospholipid bilayer in the
enelope membranes.
Special proteins called &TP !ynthetase do allow 4
E
to pass
through them and escape into the mitochondrial matri$.
Fheneer an 4
E
ion moes through the AT' Synthetase protein
an A.' is phosphorylated by the AT' Synthetase.
!n summary7
+. /A.4 and #A.4
)
contain stored chemical energy
). The energy is used to pump 4
E
into the mitochondrial
membrane against the concentration gradient
5. 4
E
trapped in one place represents a store of potential
energy
<. 4
E
ions leae the enelope through AT' Synthetase
proteins.
&. The potential energy of the 4
E
is used to phosphorylate
AT' as the 4
E
moes out of the enelope
5.9.9
!n anaerobic respiration lactate is taken ia the blood to the lier,
where it is broken down into pyruate using o$ygen and /A.4.
55
5(
c h e m o r e c e p t o r s i n
a o r t i c a n d c a r o t i d
b o d i e s
c h e m o r e c e p t o r s i n
m e d u l l a
s t r e t c h r e c e p t o r s
i n m u s c l e s
c o r t e x
( v o l u n t a r y c o n t r o l )
R E S P I R A T O R Y
E ! T R E
i n m e d u l l a o " b r a i n
d i a p h r a # m
i n t e r c o s t a l
m u s c l e s
s t r e t c h
r e c e p t o r s
i n t e r c o s t a l
n e r v e
p h r e n i c
n e r v e v a g u s
n e r v e
p r e s s u r e
r e c e p t o r s i n a o r t i c
a n d c a r o t i d
b o d i e s
c h e m o r e c e p t o r s i n
a o r t i c a n d c a r o t i d
b o d i e s
t e m p e r a t u r e
r e c e p t o r s i n
m u s c l e s
s t r e t c h r e c e p t o r s
i n m u s c l e s
v a s o c o n s t r i c t i o n
a n d
v a s o d i l a t i o n
s i n o a t r i a l
n o d e
p a r a s y m p a t h e t i c
n e r v e
( i n h i b i t o r )
A R $ I O % A S & ' A R
E ! T R E
i n m e d u l l a o " b r a i n
s y m p a t h e t i c
n e r v e
( a c c e l e r a t o r )
5.9.:
5.9.<
A spirometer is used to plot breathing patterns
9ital 6apacity: The ma$imum amount of air a person can e$hale
after inhaling the ma$imum possible olume of
air
Tidal 9olume: The olume of air inhaled = e$haled in one
breath
"asal (etabolic ;ate: The rate of respiration
The spirometer can be used to plot 96 and T9 directly. "(; can be
worked out if a 6O
)
scrubber is used. The spirometer has fi$ed olume
and is filled with +,,I O
)
before the e$periment begins. As the person
respires, O
)
is replaced proportionally with 6O
)
. The total olume should
stay constant. 4oweer, if 6O
)
is remoed, the total olume will slowly fall
as O
)
is used. The rate at which the olume decreases is proportionaly to
"(;.
Dou are not e$pected to know how the spirometer worksY although its not
ery difficult to understand.
5.9.1= @ 5.9.11
Sprinters need lots of fast twitch muscle, Coggers need slow twitch.
Therefore, the muscle type of a cheetah or a ga@elle will be
predominantly )ast twitch, whereas the muscle of a camel or an elephant
will be predominantly slow twitch.
(uscle type in humans is predominantly one or the other due to inherited
alleles. 4oweer, different training programmes can cause the I of
either type to change slightly.
5)
T9
&.0.+)
See <.K.++ for mechanisms of thermoregulation.
The thermoregulatory process (and most homeostatic systems) are
controlled by negati$e )eed.ack processes. !f a system changes, it
is detected, a homeostatic response is actiated, which aims to
return the system to its original leel. /egatie feedback,
therefore, holds systems at a set point, in this case 50.&Q6.
5.9.1/
'ositie effects of e$ercise include7
+. !ncreased "(;
). .ecreased blood pressure
5. !ncreased 4.-
<. .ecreased -.-
5*
!low twitch )i.res Fast twitch )i.res
;ed (lots of myoglobin) Fhite (little myoglobin
(any mitochondria #ew mitochondria
-ittle sarcoplasmic reticulum -ots of sarcoplasmic reticulum
-ow glycogen content -ots of glycogen
/umerous capillaries #ew capillaries
#atigue resistant #atigue ?uickly
A moderate leel of e$ercise
improes health = well*being.
4oweer, oer*training can result
in the opposite effect. This is the
phenomenon known as Gburn*outH
&. (aintaining healthy "(!
K. .ecreased risk of diabetes
0. !ncreased bone density
L. !mproed well being
M. .ecreased adrenaline leels
+,.-ess stress
++. .ecreased risk of 64.
+).(oderate e$ercise increases leels of 6atural Killer cells,
which secrete apoptosis*inducing chemicals in response to
non*specific iral or cancerous threat
/egatie effects of e$ercise (oer*training) include7
+. .ecreased leels of /atural 3iller 6ells, 'hagoctyes and " = T
6ells. This decreses immune response.
). !ncreased muscle inflammation
5. (uscle tears and sprains
<. !ncreased adrenaline leels
&. !ncreased cortisol leels, which also decreases the immune
response
K. !ncreased stress
0. .amaged cartilage
L. Tendinitis
M. -igament damage
+,.Swollen bursae
5.9.14
3ey*hole surgery is a techni?ue which allows doctors to conduct
surgery with the minimum possi.le damage to the patient. The
surgeon makes a small incision (a Gkey*holeH) and uses a fibre*optic
camera to iew the damaged area. !f re?uired, the surgeon can
make a second incision and use a number of small, remote operated
tools to repair the damage. "ecause the incisions are small and only
the damaged area is targeted, the patient recoers ?uickly. There is
also less chance of infection.
5%
%nfortunately, the procedure re?uires a high degree of training,
e$pensie e?uipment and can only be used on certain types of
surgery.
'rosthetics allow people with amputations to participate in many
actiities, including sports.
5.9.15
Fhy should we allow use of drugs7
:ies people a chance to be as good as their potential allows
;emoes GunfairH genetic adantages
6ontrolled use of drugs is less risky
'eople should hae the right of choice
-egalising drugs makes their distribution controllable (no use
by under*age, infirm etc)
Arguments for not using drugs7
.angerous (obiously)
(ay be pushed onto athletes by trainers
1ffects are permanent
(+
,rug 0))ect on physiology 0))ect on per)ormance !ideAe))ects
1rythropoietin
(1'O)
1'O causes the bone marrow
to generate e$tra red blood
cells.
1$tra blood cells mean the
blood can carry e$tra o$ygen.
This increases the leel of
work the body can sustain
through aerobic respiration
(aerobic threshold).
!ncreased haemocrit
increases blood
iscosity. This causes
strain on the heart
and can lead to
infarction
6reatine 6reatine combines with
phosphate to form 6reatine
'hosphate (6'). 6' can
phosphorylate A.', re*
generating AT'.
"ecause AT' is re*generated
without using the respiratory
pathways, theoretically it
should increase the ma$imum
power of muscles and decrease
recoery time
.iarrhoea , omiting,
lier damage and
kidney damage.
Testosterone "inds to androgen receptors
in target cells and increases
transcription of anabolic
proteins (growth proteins)
such as actin = myosin.
(uscle mass increases, which
makes the athlete more
powerful. !t also decreases
recoery time.
Agression, decreased
se$ drie, infertility,
skin problems, acne,
shrunken testicles
/ot used under doctor2s superision
Often cut with other drugs
1$poses athletes to criminals (danger of using other drugs)
The list goes on, Cust think for yourself in the conte$t of the
?uestion. Dou can argue the toss either way, but make sure you can
back up your opinion with some sensible, logical arguments.
(1
Unit 5: Energy, Exercise and
Coordination
Topic :: rey matter
5.:.1
Sensory nere: carries electrical message from receptor to spine
(otor nere: carries electrical message from spine to effector
;elay nere: connects sensory and motor neres. Also relays
message to the brain.
Schwann cells: wrap around the a$on of the long neres, creating
a thick layer of membrane, which insulates the
nere and allows for much faster conduction
speed. The thick layer of membrane has gaps in it
between adCacent Schwann cells, these are called
/odes o) 2an$ier.
5.:.%
(2
SNAB A2 Revision Notes
5.:./
Se?uence of eents in an action potential7
(3
*igh light intensity
6ircular muscles: contracted
;adial muscles: rela$ed
'upil diameter: small
7ow light intensity
6ircular muscles: rela$ed
;adial muscles: contracted
'upil diameter: large
9oltage*:ated 3
E

6hannels open
9oltage*:ated /a
E

6hannels open
/ere is
hyperpolarised and
inactie (refractory
period)
The &ction Potential
+. /ere is at resting membrane potential (*0,m9)
). A stimulus depolarises the nere to threshold (*&,m9)
5. FoltageAgated 6a
;
Channels open
<. Sodium floods into the cell and the membrane potential
depolarises to E5,m9
&. FoltageAgated K
;
Channels open
K. 'otassium floods out of the cell and the membrane potential
falls to *M,m9
0. The nere is in the refractory period and cannot conduct
another action potential
L. The /6a
;
I%K
;
&TPase C6a
;
IK PumpD restores the ion
concentrations
M. The nere is ready to fire again
As one part of the nere fires off, /a
E
diffuses into the ne$t
section of the nere, which depolarises the nere to threshold. This
se?uence is repeated like a tiny (e$ican wae down the a$on of the
nere.
/odes of ;anier speed this conduction process up. Fhen one node
depolarises it induces the ne$t section of the nere to depolarise by
forming a mini*circuit between nodes. This causes the action
potential to GCumpH between nodes of ranier, making conduction
speed much faster.
5.:.4
A synapse is the Cunction between two neres. !t is also a erb, i.e.
one nere synapses with another (meaning, passes a message to
another).
The neurotransmitter on your syllabus is Ach, but oer ),,, other
transmitters hae been discoered
(4
+. The wae of depolarisation arries at the synaptic knob. The
membrane in the presynaptic neuron is depolarised to B&,m
(threshold potential) and the oltage*gated /a
E
channels
open, letting /a
E
into the cell.
). The membrane is depolarised to E5,m9 and oltage*gated 3
E
channels open. The membrane potential falls to BM,m9 and
the cell goes into its refractory period, where the 5/a
E
8)3
E
*
AT'ase restored the ion concentrations.
5. %nlike a$ons, presynaptic neres also contain a FoltageA
gated Ca
%;
channel. As the presynapstic membrane
depolarises these channels open and let 6a
)E
into the cell.
<. The 6a
)E
causes esicles in the presynaptic nere to migrate
and fuse with the presynaptic membrane, where they spill
neurotransmitter chemical into the synaptic cleft.
(5
/
4
%
1
5
9
8
&. The neurotransmitter (&cetyl Choline) diffuses across the
cleft and binds to receptors on the postsynaptic membrane.
K. The receptors let a little /a
E
into the postsynaptic neuron,
which is enough to initiate another action potential in the
postsynaptic nere.
0. The A6h is broken down by an en@yme called &cetyl Choline
0sterase (Ach1), which allows the postsynaptic receptors to
be freed ready for a second synapse.
!n a neuromuscular Cunction the se?uence of eents in the
synapse is e$actly the same. The only difference is that the
posysynaptic nere is a muscle cell and, instead of being flat,
the postsynaptic membrane has deep grooes (t tubules) which
allow the depolarisation to spread ?uickly through the muscle
so all parts of the muscle contract at the same time.
Some neurotransmitters can hyperpolarise postsynaptic
neres, which essentially switches them off. An e$ample of
this type of inhi.itory neurotransmitter is &#&
5.:.5
Fisual transduction is the process by which light initiates a nere
impulse. The structure of a rod cell is:
The detection of light is carried out on the membrane disks in the
outer segment. These disks contain thousands of molecules of
((
rhodopsin, the photoreceptor molecule. ;hodopsin consists of a
membrane*bound protein called opsin and a coalently*bound
prosthetic group called retinal. ;etinal is made from itamin A, and
a dietary deficiency in this itamin causes night*blindness (poor
ision in dim light). ;etinal is the light*sensitie part, and it can
e$ists in ) forms: a cis form and a trans form:
!n the dark retinal is in the cis form, but when it absorbs a photon
of light it ?uickly switches to the trans form. This changes its shape
and therefore the shape of the opsin protein as well. This process is
called .leaching. The reerse reaction (trans to cis retinal) re?uires
an en@yme reaction and is ery slow, taking a few minutes. This
e$plains why you are initially blind when you walk from sunlight to a
dark room: in the light almost all your retinal was in the trans form,
and it takes some time to form enough cis retinal to respond to the
light indoors.
;od cell membranes contain a special sodium channel that is
controlled by rhodopsin. ;hodopsin with cis retinal opens it and
rhodopsin with trans retinal closes it. This means in the dark the
channel is open, allowing sodium ions to flow in and causing the rod
cell to be depolarised. This in turn means that rod cells release
neurotransmitter in the darkN
4oweer the synapse with the bipolar cell is an inhi.itory synapse,
so the neurotransmitter stops the bipolar cell making a nere
impulse. !n the light eerything is reersed, and the bipolar cell is
depolarised and forms a nere impulse, which is passed to the
ganglion cell and to the brain.
()
Summary for light7
+. 'hoton hits rhodopsin
). "leaching occurs and trans retinal is formed
5. Trans retinal blocks /a
E
channels
<. The rod is hyperpolarised and stops releasing inhibitory
neurotransmitter
&. The bipolar cell is no longer inhibited and depolarises
K. The ganglion cell is actiated, which carries the message to
the brain
6ones work in e$actly the same way, e$cept that they contain the
pigment -odopsin, which is found in 5 different forms7 red*
sensitie, blue*sensitie and green*sensitie. This gies us colour
ision.
5.:.8
*omeostasis is the maintenance of the internal enironment.
* /ere refle$es gie immediate responses
* 4ormone responses gie responses oer weeks B months
(*
4ormones are released from glands, which release hormone into the
blood. The hormone is carried all oer the body. !t binds to hormone
receptors on cell membranes and initiates responses in those cells.
5.:.9
*ind.rain
#rainstem B %ppermost part of the spine, where the spine Coins the
brain
+edulla * controls ital Whousekeeping2 functions, such as heartbeat,
blood pressure and peristalsis.
(%
.ere'ellum
Brainstem
:i#'rain
.ere'rum
:e#ulla
Cere.ellum A controls muscle co*ordination = learns motor
programmes (e.g. like how to ride a bike, or write).
+id.rain:
Thalamus B a relay station that carries sensory information from
the sense organs to the correct part of the corte$ and
hypothalamus. The thalamus contains the !uperior Collicului, which
control the initial processing of isual information. The Superior
6olliculi control obCect tracking, spatial position and partial
recognition (i.e. whether a stimulus is food or a threat)
*ypothalamus B receies sensory information from the thalamus.
6ontains homeostatic centres, which control factors like body
temperature and blood osmolarity. The hypothalamus is connected
to the 'ituitary gland and therefore the hypothalamus can stimulate
the release of a great number of pituitary hormones
Fore.rain:
Corte" B processes sensory information and controls the body2s
oluntary behaiour, i.e. learning, personality and memory.
This is the part of the brain that actually Gthinks.H The corte$ is
ery large in humans and is folded to increase the surface area
further. Other animals hae roughly similar si@e hind* and
midbrains. 4oweer, their corte$ is much, much smaller.
)+
4Spee2h motor
area9
!u#itory
asso2iation area
Premotor
Somatosensory
/isual
asso2iation area
Occipital lo.e * processes = interprets information from the
eyes
Temporal lo.e * processes = interprets information from the
ears and processes language and the meaning of words
Parietal lo.e B processes and interprets information about
touch, taste, pressure, pain, heat and cold. Also initiates motor
commands.
Frontal lo.e * plans and organises thought, is inoled with
short term memory and puts speech together.
5.:.:
)1
(%nderstanding language)
Techni1ue *ow it works 4hat it allows us to see
Surgery
.uring brain surgery a local
anaesthetic is often used. This
allows the surgeon to ask the
patient ?uestions as he
operates on their brain
The patient can tell the doctor
what he8she is feeling as the
doctor stimulates parts of
his8her brain. This can tell us a
lot about the function of the
brain.
6 T Scan
Thousands of narrow*beam S*
rays pass through the patient2s
head from a rotating source.
The rays are collected on the
other side of the head and
their strength measured. The
density of the tissue the Sray
passes through decreases the
strength of the signal, and
therefore, lets us work out
what type of tissue is in the
brain.
6T Scans show brain structures,
not brain actiity. They also only
gie Gfro@enH still images.
4oweer, they are ery useful
for picking up diseases, such as
cancer, stroke and oedema.
(;! Scan
(agnetic fields are used to
align protons in water molecules
in the patients brain. Fhen the
fields are switched off, the
protons gie out a little energy,
which can be detected.
"y recording the energy gien
out by protons we can build up a
se?uence of thin pictures of the
types of tissues inside the brain.
This can be fed into a computer,
which uses the picture to build up
a 5. image of the inside of the
head
f(;! Scan
9ery similar to aboe, e$cept
that the magnetic fields are
tuned to e$cite deo$ygenated
haemoglobin. This shows up all
the areas in the brain where
o$ygen is being used
As aboe, .ut the doctor not only
knows what the tissues look like,
but whether they are acti$e.
This is the only techni?ue, that
shows brain actiity.
5.:.<
4ow to process stimuli correctly must be learned. The corte$ is
split into column of cells. Fhen we are born, the columns oerlap
and are tangled. As we learn to process stimuli, the cells organise
themseles into discrete columns, which no longer oerlap. There is
a Gcritical windowH for this to happen (usually before puberty,
)2
younger for isual processing). !f we miss the window, our brains will
become Gfi$edH with tangled columns and won2t be able to process
stimuli properly.
*u.el @ 4ieselHs e$periments proe this.
5.:.1=
The (uller*-yer illusion7
-ines A and " are the same length, yet look different B whyO The
answer is that you hae learned to process this kind of stimuli in a
certain way. Fe lie in a Gcarpentered worldH of straight lines and
we interpret line " as a corner (therefore larger than it appears,
because it must be far away) and line A as a corner (therefore,
smaller than it appears, because it must be close).
These optical illusions do not work on Aulus, which proes the
illusion is caused by learned $isual processing, rather than an innate
function of the eye 8 brain.
5.:.11
Association (classical conditioning):
%S %; (#ood Saliation)
)3
Oer time, if a neutral stimulus (6;) is played with the %S, it
becomes associated with the %S and begins to elicit the same
response. 1entually, the animal learns
6S 6; ("ell Saliation)
'aloian conditioning occurs by synapses between neres growing
together. This means that the sensory nere carrying the message
of the 6S will always lead to the firing of the motor nere, which
triggers the 6;.
Operant 6onditioning:
This is ery similar to classical conditioning e$cept the animal learns
by doing something i.e. it learns that an action has a certain
outcome
A O (pushing a leel food)
4abituation:
!f the neutral stimulus is continuously present (not Cust before the
%S), but all the time, the animal learns to ignore the 6S. The animal
learns the bell signals nothing and it ignores the 6S totally. This is
called ha.ituation.
!f a nere is fre?uently stimulated, the amount of 6a
)E
that enters
the pre*synaptic nere gradually diminishes, until it is no longer
enough to trigger esicles to fuse with the pre*synaptic membrane.
This means no neurotransmitter is released, which results in no
post*synaptic depolarisation. The effect is, essentially, that the
stimulus is ignored.
!nsight -earning:
!n the early +M,,s, Folfgang 3ohler performed insight e$periments
on chimpan@ees. 3ohler showed that the chimpan@ees sometimes
)4
used insight instead of trial*and*error responses to sole problems.
Fhen a banana was placed high out of reach, the animals discoered
that they could stack bo$es on top of each other to reach it. They
also reali@ed that they could use sticks to knock the banana down.
!n another e$periment, a chimp balanced a stick on end under a
bunch of bananas suspended from the ceiling, then ?uickly climbed
the stick to obtain the entire bunch intact and unbruised (a better
techni?ue than the researchers themseles had in mind). 3ohler[s
e$periments showed that primates can both see and use the
relationships inoled to reach their goals.
This type of learning is ery difficult to e$plain using the 'aloian
model of conditioning. !t is also difficult to e$plain using neuronal
models of learning (i.e. synapses growing together through use)
deeloped through studies on Aplysia. 4ow insight learning occurs is
unknown at the moment.
5.:.1%
'alo2s .ogs
'alo had obsered that an unconditioned stimulus causes an
unconditioned response, i.e. food causes saliation. This is not
learned and is, therefore, unconditioned.
Fhat 'alo discoered was that if a neutral stimulus, such as a bell
is rung Cust before the food is gien for a few occasions, the dog
will saliate eery time the bell is rung, een if no food is presented.
!n this case, the dog has learned that the bell signals food. The
food is, therefore, a conditioned stimulus and it prompts a
conditioned response.
%S %;
%S E 6S %;
1entually, 6S 6;
4ubel = Fiesel
)5
4ubel = Fiesel2s (ethod:
+. ;aise monkeys from birth in three groups for 8 months
). :roup + are the control (no blindfold), :roup ) are blindfolded
in both eyes, :roup 5 are blindfolded in one eye (monocular
depri$ation)
5. Test the monkeys to see whether they can see using each eye
<. Test the sensitiity of retinal cells
&. Test the actiity of neres in the isual corte$ in response to
stimuli
The results:
(onkeys in :roup ) (both eyes blindfolded) had impaired
ision
(onkeys in :roup 5 (monocular depriation) were blind in the
depried eye
;etinal cells were responsie in all groups
6ortical actiity was reduced in parts of the brain that
process information from the depried eye
Adults undergoing the same tests showed no difference
between groups. All could see.
)(
*u.el @ 4iesel inestigated
the critical window.
They used monkeys and kittens
in their studies
Their work permanently blinded
some animals and can be argued
to be unethical.
'ermanently
blind
monkeysO
The 6onclusion:
There is a critical window for isual neural deelopment, which
re?uires stimulus from the eye. !f this window is missed the monkey
is blind, because of eents happening in the brain, not the eye.
Dou need to know about these e$periments because they all use
animals
5.:.1/
5.:.14
!n ParkinsonHs disease neurons in the brain die. All these neurons
secrete dopamine neurotransmitter, which causes difficulty in
moement and limb shaking.
!n depression neurons in the brain that secrete serotonin
neurotransmitter stop working properly and serotonin leels fall.
))
&rguments &gainst &rguments For
6linical Trials Stage + inoles animals.
Fithout animals we would not be able
to discoer new drugs
Animal testing is better than nothing
and does, in some cases, aert
potential loss of human life
Etilitarian argument: Animal testing
is for the greater good
(achines like the (;! were unested
using animals.
Animal testing has adanced our
understanding of human physiology
Fhy not use computer simulations in
6linical trials insteadO
Animal physiology is different to human
physiology. Animal testing is, therefore,
unhelpful
Animals hae rights too.
Animals hae no in)ormed consent
Testing on animals when the potential
side*effects are unknown is immoral.
Animals can2t tell you when they are
suffering
Animals are often poorly cared for in
labs
!n both cases treatments that increase the leels of
neurotransmitter might proe successful in relieing the symptoms
of these diseases
5.:.15
.rugs that affect synapses can drastically alter the functioning of
the brain7
(.(A:
Actie ingredient in ecstasy. This binds to protein pumps on the
pre*synaptic membrane of neres that secrete serotonin. The
pumps would normally take serotonin up after it had been released,
therefore reducing firing in post*synaptic neres. #ET, when these
channels are blocked, serotonin builds up in the cleft, giing greater
post*synaptic actiation and a sense of euphoria.
-*.opa:
This is a precursor of dopamine. Fhen gien to 'arkinson2s
sufferers it is turned into dopamine, which helps alleiate some of
the symptoms of the disease.
5.:.18
Continuous $ariation: there is a wide range of phenotypes (e.g.
height)
,iscontinuous $ariation: phenotypes fall into discrete categories
(e.g. blood type)
.iscontinuous ariation tends to be coded for by one gene with a
few different alleles. 4oweer, continuous ariation is more
comple$. This is usually coded for by many genes (polygenes), with
many alleles, which produces the much greater range of possible
phenotypes.
)*
'olygenes can gie rise to susceptibility to disease, usually with an
enironmental trigger. .iseases that are both genetic and
enironmental are called multi)actorial
5.:.19
"rain deelopment is a combination of nature and nurture.
)%