Behavioral Biology

Neural Systems of Reinforcement for Drug Addiction: From Actions to Habits to Compulsion and from Ventral to Dorsal Striatum.- Impact of Basic Research on Clinical Practice Clinical and Preclinical Perspectives.- Cell Genesis and Migration in the Basal Ganglia in Health and Disease.- Oscillations in the Basal Ganglia Network: Cellular Mechanisms and Pathological Aspects.- Stem Cells.- Up-Down States.- Deep Brain Stimulation.- Respecting Your Elders: Why Subcortical Connections with the Basal Ganglia are Important.- Understanding Mechanisms of L-Dopa Induced Side-Effects.- Behavioral Correlates of Basal Ganglia Function and Dysfunction.- Computational Models of the BG: From Molecules and Membranes to Behaviour and Cognition.- Genetic Aspects of Movement Disorders.- Basal Ganglia, Reward and Drug Seeking.- Index.

One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).

Reactive oxygen and nitrogen species may cause various types of chemical modifications on specific proteins, Such modifications if irreversible are often associated with permanent loss of function and may lead to the elimination or to the accumulation of the damaged proteins. Reversible modifications, particularly at the cysteine residues, may have a dual role of protection from cysteine irreversible oxidation and modulation of protein function (redox regulation). Here we will review the techniques available for identifying proteins based on their redox state. In particular, we will focus on protein carbonylation, tyrosine nitration and thiol-disulfide chemistry of cysteines, with special emphasis on glutathionylation, because these are the fields where the tools of proteome analysis have been applied.

... Titre du document / Document title. Ubiquitin in Alzheimer and other neurodegenerative diseases. Auteur(s) / Author(s). PERRY G. (1) ; MANETTO V. ; MULVIHILL P. ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s). (1) Case western reserve univ., inst. ...

The neuron, like many other types of cells, contains three major morphologically distinct filamentous systems: microfilaments, intermediate filaments and microtubules.1 The role of these cytoskeletal components in the neuron has been unclear until recently. These discoveries have implicated the cytoskeleton in many cell functions, including internal organization.2–5 Microfilaments in neurons have mainly been studied in relation to axonal transport.6–9 By light microscopy, actin filaments have been demonstrated in neurites,10–13 growth cones of avian dorsal root ganglia cells14–18 and in microspikes of murine neuroblastoma cells.10–11 In situ organization of actin filaments in dendritic spines, dendrites and axon terminals has been demonstrated19 using heavy meromyosin decoration.20

Collecting human brain for research on Alzheimer's disease (AD) and related disorders should put emphasis on the development of a rapid autopsy system, eg, as practised by the Netherlands Brain Bank (NBB) and guarantee the quality of the tissue by proper matching and measuring the pH of the brain or cerebrospinal fluid (CSF)(Ravid and Swaab, 1993; Ravid et al., 1992). Specimens from diseased and control brains are properly matched for the various ante and post-mortem factors in addition to Apo-E typing and the quality of the ...

The voltage dependent sodium current determines the upstroke of the action potential, and it is therefore one of the determinant factors for neuronal excitability. The steep voltage dependence of activation as well as inactivation in combination with its fast kinetics imply that even relatively small changes in sodium current properties will have a significant influence on, for example, cell firing frequency. It is therefore not surprising that the majority of antiepileptic drugs (AEDs) exert their action by modulating sodium current properties that are relevant for cell firing.1 The aim of this study is to parameterize the sodium current in CA1 hippocampal pyramidal cells using the classical description originally provided by Hodgkin and Huxley2, 3 employing voltage clamp data obtained from neurons acutely isolated from the rat hippocampus. Such a description does not comprise every possible detail of the present knowledge of the sodium channel. Nevertheless it appears to be sufficient to describe the changes observed in the inactivation function of the sodium current in neurons isolated from the epileptic focus in rats that were either kindled4 or in which a status epilepticus model was generated.5

... Cholinergic-Amyloid Fusion Hypothesis Thomas Beach, Pamela Potter, Lucia Sue, Amanda Newell, Marissa Poston, Raquel Cisneros, Yoga Pandya, Abraham Fisher, Alex Roher, Lih-Fen Lue, and Douglas Walker Introduction ... 15. Beach TG, Potter PE, Kuo YM, et al. ...