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Hippocampal area CA2: interneuron disfunction during pathological states

Hippocampal area CA2 plays a critical role in social recognition memory and has unique cellular and molecular properties that distinguish it from areas CA1 and CA3. In addition to having a particularly high density of interneurons, the inhibitory transmission in this region displays two distinct for...

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Autores principales: Piskorowski, Rebecca A., Chevaleyre, Vivien
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10174260/
https://www.ncbi.nlm.nih.gov/pubmed/37180763
http://dx.doi.org/10.3389/fncir.2023.1181032
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author Piskorowski, Rebecca A.
Chevaleyre, Vivien
author_facet Piskorowski, Rebecca A.
Chevaleyre, Vivien
author_sort Piskorowski, Rebecca A.
collection PubMed
description Hippocampal area CA2 plays a critical role in social recognition memory and has unique cellular and molecular properties that distinguish it from areas CA1 and CA3. In addition to having a particularly high density of interneurons, the inhibitory transmission in this region displays two distinct forms of long-term synaptic plasticity. Early studies on human hippocampal tissue have reported unique alteration in area CA2 with several pathologies and psychiatric disorders. In this review, we present recent studies revealing changes in inhibitory transmission and plasticity of area CA2 in mouse models of multiple sclerosis, autism spectrum disorder, Alzheimer’s disease, schizophrenia and the 22q11.2 deletion syndrome and propose how these changes could underly deficits in social cognition observed during these pathologies.
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spelling pubmed-101742602023-05-12 Hippocampal area CA2: interneuron disfunction during pathological states Piskorowski, Rebecca A. Chevaleyre, Vivien Front Neural Circuits Neural Circuits Hippocampal area CA2 plays a critical role in social recognition memory and has unique cellular and molecular properties that distinguish it from areas CA1 and CA3. In addition to having a particularly high density of interneurons, the inhibitory transmission in this region displays two distinct forms of long-term synaptic plasticity. Early studies on human hippocampal tissue have reported unique alteration in area CA2 with several pathologies and psychiatric disorders. In this review, we present recent studies revealing changes in inhibitory transmission and plasticity of area CA2 in mouse models of multiple sclerosis, autism spectrum disorder, Alzheimer’s disease, schizophrenia and the 22q11.2 deletion syndrome and propose how these changes could underly deficits in social cognition observed during these pathologies. Frontiers Media S.A. 2023-04-27 /pmc/articles/PMC10174260/ /pubmed/37180763 http://dx.doi.org/10.3389/fncir.2023.1181032 Text en Copyright © 2023 Piskorowski and Chevaleyre. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neural Circuits
Piskorowski, Rebecca A.
Chevaleyre, Vivien
Hippocampal area CA2: interneuron disfunction during pathological states
title Hippocampal area CA2: interneuron disfunction during pathological states
title_full Hippocampal area CA2: interneuron disfunction during pathological states
title_fullStr Hippocampal area CA2: interneuron disfunction during pathological states
title_full_unstemmed Hippocampal area CA2: interneuron disfunction during pathological states
title_short Hippocampal area CA2: interneuron disfunction during pathological states
title_sort hippocampal area ca2: interneuron disfunction during pathological states
topic Neural Circuits
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10174260/
https://www.ncbi.nlm.nih.gov/pubmed/37180763
http://dx.doi.org/10.3389/fncir.2023.1181032
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