Fiche publication
Date publication
juillet 2017
Journal
Progress in neuro-psychopharmacology & biological psychiatry
Auteurs
Membres identifiés du Cancéropôle Est :
Dr HERAULT Yann
Tous les auteurs :
Aincy M, Meziane H, Herault Y, Humeau Y
Lien Pubmed
Résumé
The amygdala is a part of the limbic circuit that has been extensively studied in terms of synaptic connectivity, plasticity and cellular organization since decades (Ehrlich et al., 2009; Ledoux, 2000; Maren, 2001; McDonald, 1982). Amygdala sub-nuclei, including lateral, basolateral and central amygdala appear now as "hubs" providing in parallel and in series neuronal processing enabling the animal to elicit freezing or escaping behavior in response to external threats. In rodents, these behaviors are easily observed and quantified following associative fear conditioning. Thus, studies on amygdala circuit in association with threat/fear behavior became very popular in laboratories and are often used among other behavioral tests to evaluate learning abilities of mouse models for various neuropsychiatric conditions including genetically encoded intellectual disabilities (ID). Yet, more than 100 human X-linked genes - and several hundreds of autosomal genes - have been associated with ID in humans. These mutations introduced in mice generate learning and memory deficits (Chelly et al., 2006; Ropers and Hamel, 2005). Noteworthy, a significant proportion of the coded ID gene products are synaptic proteins. It is postulated that the loss of function of these proteins could destabilize neuronal circuits by global changes of the balance between inhibitory and excitatory drives onto neurons. However, whereas amygdala related behavioral deficits are commonly observed in ID models, the role of most of these ID-genes in synaptic function and plasticity in the amygdala are only sparsely studied. We will here discuss some of the concepts that emerged from amygdala-targeted studies examining the role of syndromic and non-syndromic ID genes in fear-related behaviors and/or synaptic function. Along describing these cases, we will discuss how synaptic deficits observed in amygdala circuits could impact memory formation and expression of conditioned fear.
Mots clés
Amygdala, pathology, Animals, Avoidance Learning, physiology, Conditioning, Classical, physiology, Disease Models, Animal, Fear, Humans, Intellectual Disability, genetics, Synapses, pathology
Référence
Prog. Neuropsychopharmacol. Biol. Psychiatry. 2017 Jul;:
