Do changes in microglial status underlie neurogenesis impairments and depressive-like behaviours induced by psychological stress? A systematic review in animal models.
Animal models
Depression
Microglia
Neurogenesis
Neuroinflammation
Psychosocial stress
Systematic review
Journal
Neurobiology of stress
ISSN: 2352-2895
Titre abrégé: Neurobiol Stress
Pays: United States
ID NLM: 101643409
Informations de publication
Date de publication:
Nov 2021
Nov 2021
Historique:
received:
29
03
2021
revised:
14
06
2021
accepted:
14
06
2021
entrez:
6
8
2021
pubmed:
7
8
2021
medline:
7
8
2021
Statut:
epublish
Résumé
Stress may have a negative effect on mental health and is the primary environmental risk factor in the aetiology of depression. Nevertheless, the neurobiological mechanisms underlying this mood disorder remain poorly characterized. The hippocampus is a target structure of the adverse effects of stress, and hippocampal neurogenesis plays a crucial role. However, we do not know the mechanisms by which stress impacts neurogenesis. Recent studies indicate that changes in neuroinflammation, primarily via microglial cells, may play an essential role in this process. However, the relationship between stress, microglial changes, and alterations in neurogenesis and their involvement in the development of depression is poorly characterized. For this reason, this systematic review aims to synthesise and evaluate current studies that have investigated the relationship between these variables. Taken together, the revised data, although not entirely conclusive, seem to suggest that microglial changes induced by psychological stress regulate neurogenesis and in turn may be responsible for the development of depressive-like behaviours, but other factors that influence these stressful experiences should not be dismissed.
Identifiants
pubmed: 34355047
doi: 10.1016/j.ynstr.2021.100356
pii: S2352-2895(21)00064-3
pmc: PMC8319800
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
100356Informations de copyright
© 2021 The Authors.
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