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Physiology of Pain

Crit Care Nurs Clin N Am 29 (2017) 397–406

Deer’s Treatment of Pain

https://doi.org/10.1007/978-3-030-12281-2
CHRONIC PAIN

Annu. Rev. Medicine 1998. 49:123–33

Deer’s Treatment of Pain

https://doi.org/10.1007/978-3-030-12281-2
Basic Science of Pain

Pain Care Essentials and Innovations

Pain: Pathways and Physiology

Clin Plastic Surg - (2019) -–-

Handbook of Experimental Pharmacology

DOI 10.1007/978-3-662-46450-2
 ESSENTIALS OF Pain Medicine

FIG. 2.1 Schematic diagram of the neurochemistry

of somatosensory processing at peripheral
sensory nerve endings. 5HT, Serotonin receptor;
A2, adenosine 2 receptor; ASIC, acid-sensing ion
channels; ATP, adenosine triphosphate; B2/B1,
bradykinin 2/1 receptors; CRH, corticotropin-
releasing hormone; EP, eiconsanoid receptor;
GABA, gamma amino butyric acid; GIRK, G-protein
coupled inward rectifying potassium channel; H1,
histamine 1 receptor; IFN, interferon; iGluR,
iontotropic glutamate receptors; IL, interleukin;
LIF, leukemia inhibitory factor; M2, muscarinic 2
receptor; mGluR, metabotropic glutamate
receptor; NGF, nerve growth factor; P2X2, ATP
activated ion channels; PAF, platelet activating
factor; PGE2, prostaglandin E2; PKA, protein
kinase A; PKC, protein kinase C; SSTR,
somatostatin receptor; TNF, tumor necrosis
factor; TrkA, tropomyosin receptor kinase A;
TRPV1, transient receptor potential vanilloid 1;
TTXr, tetrodotoxin resistant (channel).

ISBN 9780323401968
Academic Pain Medicine

https://doi.org/10.1007/978-3-030-18005-8
Basic Science of Pain

Pain Care Essentials and Innovations

Basic Science of Pain

Pain Care Essentials and Innovations

Basic Science of Pain

Pain Care Essentials and Innovations

ESSENTIALS OF Pain Medicine

ISBN 9780323401968
Food, pain, and drugs: Does it matter what pain patients eat?

Pain 153 (2012) 1993–1996

Molecular mechanisms of nociception

NATURE | VOL 413 | 13 SEPTEMBER 2001

Pain as a channelopathy

J Clin Invest. 2010;120(11):3745-3752

Deer’s Treatment of Pain

https://doi.org/10.1007/978-3-030-12281-2
Pain: Pathways and Physiology

Clin Plastic Surg - (2019) -–-

Neuropathic Pain: Central vs. Peripheral Mechanisms

Curr Pain Headache Rep (2017) 21:28

Physiology of Pain

Crit Care Nurs Clin N Am 29 (2017) 397–406

Basic Science of Pain

Pain Care Essentials and Innovations

Neuropathic Pain: Delving into the Oxidative Origin and the Possible Implication of Transient Receptor Potential Channels

Front. Physiol. 9:95

Neuropathic Pain: Delving into the Oxidative Origin and the Possible Implication of Transient Receptor Potential Channels

Front. Physiol. 9:95

Etiology and Pharmacology of Neuropathic Pain

Pharmacol Rev 70:315–347, April 2018

Etiology and Pharmacology of Neuropathic Pain

Pharmacol Rev 70:315–347, April 2018

Chronic Pain: Pathophysiology and Mechanisms

Essentials of Interventional Techniques in Managing Chronic Pain

Pain chronification: what should a non-pain medicine specialist know?

Current medical research and opinion 2018, VOL. 34, NO. 7, 1169–1178
Pattern recognition receptors in chronic pain: mechanisms and therapeutic implications

European Journal of Pharmacology DOI: http://dx.doi.org/10.1016/j.ejphar.2016.06.039

Pattern recognition receptors in chronic pain: mechanisms and therapeutic implications

European Journal of Pharmacology DOI: http://dx.doi.org/10.1016/j.ejphar.2016.06.039

Pattern recognition receptors in chronic pain: mechanisms and therapeutic implications

European Journal of Pharmacology DOI: http://dx.doi.org/10.1016/j.ejphar.2016.06.039

Pathobiology of Visceral Pain: Molecular Mechanisms and Therapeutic Implications III. Visceral afferent pathways: a source of new therapeutic
targets for abdominal pain

Am J Physiol Gastrointest Liver Physiol 278: G670–G676

 Regulation of pain by neuro-immune interactions between macrophages and nociceptor sensory neurons

Regulation of pain induction via macrophage-

nociceptor interactions. (a) In macrophages,
activation of TLRs (e.g. TLR4 and TLR9) by PAMPs
and DAMPs increases the synthesis and release of
inflammatory cytokines and chemokines (e.g. TNF,
IL-1b, CCL2, CXCL1) and lipid mediators (e.g. PGE2)
via MyD88 and NF -kB. PAMP and DAMP can be
induced by bacteria infection, tissues injury, or
chemotherapy (e.g. paclitaxel). These inflammatory
mediators act on their respective receptors (e.
mediators to pain (Figure 3), as well as itch, a
distinct sensation that triggers scratching [9,10].
After sensing these noxious stimuli, action
potentials initiated at the peripheral terminals of
nociceptors are carried forward to 2nd order
nociceptive neurons in the dorsal horn of the spinal
cord or brain stem via their central projections.

Current Opinion in Neurobiology 2019, 62:17–25

 Regulation of pain by neuro-immune interactions between macrophages and nociceptor sensory neurons

Regulation of pain induction via macrophage-nociceptor interactions. (a) In macrophages, activation of TLRs (e.g. TLR4 and TLR9) by PAMPs and DAMPs
increases the synthesis and release of inflammatory cytokines and chemokines (e.g. TNF, IL-1b, CCL2, CXCL1) and lipid mediators (e.g. PGE2) via MyD88
and NF -kB. PAMP and DAMP can be induced by bacteria infection, tissues injury, or chemotherapy (e.g. paclitaxel). These inflammatory mediators act
on their respective receptors (e. mediators to pain (Figure 3), as well as itch, a distinct sensation that triggers scratching [9,10]. After sensing these
noxious stimuli, action potentials initiated at the peripheral terminals of nociceptors are carried forward to 2nd order nociceptive neurons in the dorsal
horn of the spinal cord or brain stem via their central projections.

Current Opinion in Neurobiology 2019, 62:17–25

Pain chronification: what should a non-pain medicine specialist know?

Current medical research and opinion 2018, VOL. 34, NO. 7, 1169–1178
Chronic Pain: Pathophysiology and Mechanisms

Essentials of Interventional Techniques in Managing Chronic Pain

Chronic Pain: Pathophysiology and Mechanisms

Essentials of Interventional Techniques in Managing Chronic Pain

Fundamentals of Pain Medicine

https://doi.org/10.1007/978-3-319-64922-1
Mechanisms of microbial–neuronal interactions in pain and nociception

Neurobiology of Pain 9 (2021) 100056

Mechanisms of microbial–neuronal interactions in pain and nociception

Neurobiology of Pain 9 (2021) 100056

Mechanisms of microbial–neuronal interactions in pain and nociception

Neurobiology of Pain 9 (2021) 100056

Prostanoids and pain: unraveling mechanisms and revealing therapeutic targets

TRENDS in Molecular Medicine Vol.8 No.8 August 2002

Prostanoids and pain: unraveling mechanisms and revealing therapeutic targets

TRENDS in Molecular Medicine Vol.8 No.8 August 2002

New Horizons in Diabetic Neuropathy: Mechanisms, Bioenergetics, and Pain

Neuron 93, March 22, 2017

Neuropathic Pain: Delving into the Oxidative Origin and the Possible Implication of Transient Receptor Potential Channels

Front. Physiol. 9:95. doi: 10.3389/fphys.2018.00095

 Pathological Mechanisms and Therapeutic Targets for Trigeminal Neuropathic Pain

Figure 2. Peripheral mechanisms of trigeminal neuropathic pain. Peripheral nerve injury releases inflammatory mediators including prostaglandin E2 (PGE2),
cytokines and neuropeptides including brain-derived neurotrophic factor (BDNF), which sensitizes peripheral nerve terminals by depolarizing nociceptors.
Expression of peripheral receptors including the transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential cation channel, subfamily
A, member 1 (TRPA1). Changes in ion channel expression and activity on trigeminal neurons increases excitability as do activated satellite glial cells (SCG),
which increase in number. Excitability of the TG neurons leads to increased release of neuropeptides substance P (SP) and calcitonin gene-related peptide
(CGRP) to postsynaptic regions in the trigeminal spinal caudalis (brain stem).

Medicines 2019, 6, 91
TRP Channel Cooperation for Nociception: Therapeutic Opportunities

Annu. Rev. Pharmacol. Toxicol. 2021. 61:19.1–19.23

 Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain—Narrative Review

Figure 1. Peripheral nerve endings, keratinocytes,

and immune cells express ion channels and
receptors and release numerous signaling molecules
to create a complex interaction, involved in
physiological nociception and neuropathic pain (NP)
generation. Abbreviations: Nav—voltagegated
sodium channels, TRP—transient receptor potential
channels, VGCCs—voltage-gated calcium channels,
NMDAR—N-methyl-D-aspartate receptors, ASIC—
acid-sensing ion channels, TLR—Toll-like receptors,
α1-AR—α1 adreno receptors, α2-AR—α2 adreno
receptors, EP— prostaglandin E2 receptors,
GABAAR—gamma-aminobutyric acid receptors A,
GABABR— gamma-aminobutyric acid receptors B,
Kv—voltage-gated potassium channels, OR—opioid
receptors, CB1, CB2—cannabinoid receptors type 1
or 2, CCL-R—chemokine receptors, IL-R—
interleukin receptors, TrkA—tropomyosin receptor
kinase A, HCN—hyperpolarization-activated cyclic
nucleotide-gated channels, P2X3—P2X
purinoceptors 3, GPCR—G protein-coupled
receptors, TLR—Toll-like receptors. Created with
BioRender.com. The recommendation for the use of
5% lidocaine patches in LNP is weak with a
moderate quality of evidence, according to the
Grading of Recommendations Assessment,
Development, and Evaluation

Pharmaceutics 2021, 13, 450

Contributions of natural products to ion channel pharmacology

Nat. Prod. Rep

Chronic Pain Management in General and Hospital Practice

https://doi.org/10.1007/978-981-15-2933-7
Pain Care Essentials and Innovations

ISBN: 978-0-323-72216-2
Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment

Lancet Neurol 2010; 9: 807–19

The neurobiology of central sensitization

J Appl Behav Res. 2018;23:e12137

Review General Pathways of Pain Sensation and the Major Neurotransmitters Involved in Pain Regulation

Int. J. Mol. Sci. 2018, 19, 2164

Review General Pathways of Pain Sensation and the Major Neurotransmitters Involved in Pain Regulation

Int. J. Mol. Sci. 2018, 19, 2164

Neuropathic pain modeling: Focus on synaptic and ion channel mechanisms

Progress in Neurobiology xxx (xxxx) xxx

Neuropathic pain modeling: Focus on synaptic and ion channel mechanisms

Progress in Neurobiology xxx (xxxx) xxx

Challenges of neuropathic pain: focus on diabetic neuropathy

Journal of Neural Transmission (2020) 127:589–624

Advances in the Treatment of Chronic Pain by Targeting GPCRs

Biochemistry XXXX, XXX, XXX−XXX

Advances in the Treatment of Chronic Pain by Targeting GPCRs

Biochemistry XXXX, XXX, XXX−XXX

Endogenous and Exogenous Opioids in Pain

Annu. Rev. Neurosci. 2018. 41:453–73

Basic Opioid Pharmacology — An Update

British Journal of Pain 1– 7

Basic Opioid Pharmacology — An Update

British Journal of Pain 1– 7

Endogenous and Exogenous Opioids in Pain

Annu. Rev. Neurosci. 2018. 41:453–73

 Endogenous and Exogenous Opioids in Pain

Figure 2
Opioid modulation of signaling and synaptic transmission. (a) Presynaptic and postsynaptic effects of opioids on nociception. (Left)Noxious stimuli trigger action potential firing along DRG nociceptors. Upon reaching the
synaptic terminal, VGCCs ( yellow) open, facilitating neurotransmitter release. These neurotransmitters (e.g., glutamate) then open postsynaptic AMPA and NMDA receptors, which continue the nociceptive signals
along pain circuits. (Right) Activation of opioid receptors promotes dissociation of inhibitory Gα and Gβγ protein subunits. Gα subunits suppress adenylate cyclase, and Gβγ subunits presynaptically inhibit VGCC opening
and postsynaptically activate GIRK channels, resulting in reduced neurotransmitter release and membrane hyperpolarization, respectively. (b) Biased signaling pathways. Agonist binding to opioid receptors causes
conformational changes that promote distinct recruitment of G protein and arrestin effector signaling cascades. While G proteins mediate the inhibitory action of opioid signaling on neurotransmission, arrestin
signaling is required both for internalization of opioid receptors and for kinase activities. The balance between G protein and arrestin signaling is thought, in part, to determine the analgesic versus detrimental effects of
opioids. (c) Within pain circuits opioid receptors are activated by opioid analgesics such as enkephalin (endogenous) or morphine (exogenous). Endogenous opioids, such as enkephalins, can be released from infiltrating
immune cells at the site of injuries and from neurons in the central nervous system. Abbreviations: AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; DRG, dorsal root ganglion; EPSC, excitatory
postsynaptic current; ERK, extracellular signal regulated kinase; GIRK, G protein inwardly rectifying potassium; JNK, c-Jun
N-terminal kinase; NMDA, N-methyl-D-aspartate; RVM, rostral ventromedial medulla; VGCC, voltage-gated calcium channel.

Annu. Rev. Neurosci. 2018. 41:453–73

 Endogenous and Exogenous Opioids in Pain

Figure 2
Opioid modulation of signaling and synaptic transmission. (a) Presynaptic and postsynaptic effects of opioids on nociception. (Left)Noxious stimuli trigger action potential firing along DRG nociceptors. Upon reaching the
synaptic terminal, VGCCs ( yellow) open, facilitating neurotransmitter release. These neurotransmitters (e.g., glutamate) then open postsynaptic AMPA and NMDA receptors, which continue the nociceptive signals
along pain circuits. (Right) Activation of opioid receptors promotes dissociation of inhibitory Gα and Gβγ protein subunits. Gα subunits suppress adenylate cyclase, and Gβγ subunits presynaptically inhibit VGCC opening
and postsynaptically activate GIRK channels, resulting in reduced neurotransmitter release and membrane hyperpolarization, respectively. (b) Biased signaling pathways. Agonist binding to opioid receptors causes
conformational changes that promote distinct recruitment of G protein and arrestin effector signaling cascades. While G proteins mediate the inhibitory action of opioid signaling on neurotransmission, arrestin
signaling is required both for internalization of opioid receptors and for kinase activities. The balance between G protein and arrestin signaling is thought, in part, to determine the analgesic versus detrimental effects of
opioids. (c) Within pain circuits opioid receptors are activated by opioid analgesics such as enkephalin (endogenous) or morphine (exogenous). Endogenous opioids, such as enkephalins, can be released from infiltrating
immune cells at the site of injuries and from neurons in the central nervous system. Abbreviations: AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; DRG, dorsal root ganglion; EPSC, excitatory
postsynaptic current; ERK, extracellular signal regulated kinase; GIRK, G protein inwardly rectifying potassium; JNK, c-Jun N-terminal kinase; NMDA, N-methyl-D-aspartate; RVM, rostral ventromedial medulla; VGCC,
voltage-gated calcium channel.

Annu. Rev. Neurosci. 2018. 41:453–73

The Contribution of the Descending Pain Modulatory Pathway in Opioid Tolerance

Front. Neurosci. 12:886

The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain

Neural Plasticity Volume 2017

The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain

Neural Plasticity Volume 2017

Management of neuropathic pain

J Gen Fam Med. 2017;18:56–60

Advances in Experimental Medicine and Biology

https://doi.org/10.1007/978-981-13-1756-9
Advances in Experimental Medicine and Biology

https://doi.org/10.1007/978-981-13-1756-9
Advances in Experimental Medicine and Biology

https://doi.org/10.1007/978-981-13-1756-9
Basic pharmacology of local anaesthetics

BJA Education, 20(2): 34e41 (2020)

Modulation of Chronic Pain by Metabotropic Glutamate Receptors

Advances in Pharmacology
Modulation of Chronic Pain by Metabotropic Glutamate Receptors

Advances in Pharmacology
Pharmacotherapy for Neuropathic Pain: A Review

Pain Ther (2017) 6 (Suppl 1):S25–S33

Pharmacotherapy for Neuropathic Pain: A Review

Pain Ther (2017) 6 (Suppl 1):S25–S33

 TRP Channels and Pain - Neurobiology of TRP Channels

ole of TRP channels in skin homeostasis and skin diseases. The skin-expressed TRP channels can
either contribute to maintaining normal skin physiology or play important roles in the
pathogenesis of skin diseases.
https://www.ncbi.nlm.nih.gov/books/NBK476120
Novel Agents in Neuropathic Pain, the Role of Capsaicin: Pharmacology, Efficacy, Side Effects, Different Preparations

Current Pain and Headache Reports (2020) 24:53

 TRP Channels and Pain - Neurobiology of TRP Channels

Figure 8.1
Transduction of pain signal. (a) Nociceptor stimulation by tissue damage. Nociceptive signals and proinflammatory compounds trigger an action
potential along the nociceptive fiber toward the central nervous system to be perceived as pain. (b) Nociceptive signals are detected by some
members of the TRP family of ion channels, which are directly activated by their agonists and indirectly by proinflammatory mediators. (DRG, dorsal
root ganglion; TG, trigeminal ganglion.)
https://www.ncbi.nlm.nih.gov/books/NBK476120
Treatment of chronic neuropathic pain: purine receptor modulation

PAIN 00 (2020) 1–17

Treatment of chronic neuropathic pain: purine receptor modulation

PAIN 00 (2020) 1–17

Histamine, histamine receptors, and neuropathic pain relief

Br J Pharmacol. 2020;177:580–599
Histamine, histamine receptors, and neuropathic pain relief

Br J Pharmacol. 2020;177:580–599
Cannabinoids in the descending pain modulatory circuit: Role in inflammation

Pharmacology & Therapeutics 209 (2020) 107495

Cannabinoids in the descending pain modulatory circuit: Role in inflammation

Pharmacology & Therapeutics 209 (2020) 107495

Cannabinoids in the Treatment of Back Pain

Neurosurgery 0:1–10, 2020

Neuropathic pain: Mechanisms and treatments

Chang Gung Med J 2005;28:597-605

 Central and Peripheral Mechanism of Acupuncture Analgesia on Visceral Pain: A Systematic Review

Figure 3: Schematic illustration of functional and metabolic changes (peptides, proteins, and mRNA) of the brain-gut axis by acupuncture in visceral pain studies. In human, acupuncture
consistently enhanced the functional activity in the thalamus and insula, the core brain regions of pain processing. In animal, a great variety of metabolic changes have been reported as
well as functional neural activities, demonstrating that acupuncture induces awide range of changes through the brain-gut axis in visceral pain.ACC: anterior cingulate cortex;AMG:
amygdala; CC: central canal; DH: dorsal horn; DRG: dorsal root ganglion; DRN: dorsal raphe nucleus; HyTH: hypothalamus; INS: insula; MED: medulla; NR2B: N-methyl-D-aspartate receptor
subunit; PAG: periaqueductal gray; PFC: prefrontal cortex; P2X3: P2X purinoceptor 3; SC: somatosensory cortex; sub P: substance P; TH: thalamus; 4th V: fourth ventricle.

Evidence-Based Complementary and Alternative Medicin Volume 2019

DOR
• Sobrevivência.
• Sinal neuronal.
• Sensibilidade.
• Lesão de tecido.
• As vezes não é requerida.
• Sem dor não existiríamos sobre a face da terra.