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Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory
A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and m...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8206813/ https://www.ncbi.nlm.nih.gov/pubmed/34149368 http://dx.doi.org/10.3389/fncir.2021.687558 |
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author | Honoré, Eve Khlaifia, Abdessattar Bosson, Anthony Lacaille, Jean-Claude |
author_facet | Honoré, Eve Khlaifia, Abdessattar Bosson, Anthony Lacaille, Jean-Claude |
author_sort | Honoré, Eve |
collection | PubMed |
description | A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and memory. Inhibitory interneurons provide more than a simple transitory inhibition of hippocampal principal cells (PCs). The synaptic plasticity of inhibitory neurons provides long-lasting changes in the hippocampal network and is a key component of memory formation. The dendrite targeting interneurons expressing the peptide somatostatin (SOM) are particularly interesting in this regard because they display unique long-lasting synaptic changes leading to metaplastic regulation of hippocampal networks. In this article, we examine the actions of the neuropeptide SOM on hippocampal cells, synaptic plasticity, learning, and memory. We address the different subtypes of hippocampal SOM interneurons. We describe the long-term synaptic plasticity that takes place at the excitatory synapses of SOM interneurons, its singular induction and expression mechanisms, as well as the consequences of these changes on the hippocampal network, learning, and memory. We also review evidence that astrocytes provide cell-specific dynamic regulation of inhibition of PC dendrites by SOM interneurons. Finally, we cover how, in mouse models of Alzheimer’s disease (AD), dysfunction of plasticity of SOM interneuron excitatory synapses may also contribute to cognitive impairments in brain disorders. |
format | Online Article Text |
id | pubmed-8206813 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82068132021-06-17 Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory Honoré, Eve Khlaifia, Abdessattar Bosson, Anthony Lacaille, Jean-Claude Front Neural Circuits Neuroscience A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and memory. Inhibitory interneurons provide more than a simple transitory inhibition of hippocampal principal cells (PCs). The synaptic plasticity of inhibitory neurons provides long-lasting changes in the hippocampal network and is a key component of memory formation. The dendrite targeting interneurons expressing the peptide somatostatin (SOM) are particularly interesting in this regard because they display unique long-lasting synaptic changes leading to metaplastic regulation of hippocampal networks. In this article, we examine the actions of the neuropeptide SOM on hippocampal cells, synaptic plasticity, learning, and memory. We address the different subtypes of hippocampal SOM interneurons. We describe the long-term synaptic plasticity that takes place at the excitatory synapses of SOM interneurons, its singular induction and expression mechanisms, as well as the consequences of these changes on the hippocampal network, learning, and memory. We also review evidence that astrocytes provide cell-specific dynamic regulation of inhibition of PC dendrites by SOM interneurons. Finally, we cover how, in mouse models of Alzheimer’s disease (AD), dysfunction of plasticity of SOM interneuron excitatory synapses may also contribute to cognitive impairments in brain disorders. Frontiers Media S.A. 2021-06-02 /pmc/articles/PMC8206813/ /pubmed/34149368 http://dx.doi.org/10.3389/fncir.2021.687558 Text en Copyright © 2021 Honoré, Khlaifia, Bosson and Lacaille. 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 | Neuroscience Honoré, Eve Khlaifia, Abdessattar Bosson, Anthony Lacaille, Jean-Claude Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title | Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title_full | Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title_fullStr | Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title_full_unstemmed | Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title_short | Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory |
title_sort | hippocampal somatostatin interneurons, long-term synaptic plasticity and memory |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8206813/ https://www.ncbi.nlm.nih.gov/pubmed/34149368 http://dx.doi.org/10.3389/fncir.2021.687558 |
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