Cargando…

Neural Circuitry–Neurogenesis Coupling Model of Depression

Depression is characterized by the disruption of both neural circuitry and neurogenesis. Defects in hippocampal activity and volume, indicative of reduced neurogenesis, are associated with depression-related behaviors in both humans and animals. Neurogenesis in adulthood is considered an activity-de...

Descripción completa

Detalles Bibliográficos
Autores principales: Kim, Il Bin, Park, Seon-Cheol
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957816/
https://www.ncbi.nlm.nih.gov/pubmed/33671109
http://dx.doi.org/10.3390/ijms22052468
_version_ 1783664736475283456
author Kim, Il Bin
Park, Seon-Cheol
author_facet Kim, Il Bin
Park, Seon-Cheol
author_sort Kim, Il Bin
collection PubMed
description Depression is characterized by the disruption of both neural circuitry and neurogenesis. Defects in hippocampal activity and volume, indicative of reduced neurogenesis, are associated with depression-related behaviors in both humans and animals. Neurogenesis in adulthood is considered an activity-dependent process; therefore, hippocampal neurogenesis defects in depression can be a result of defective neural circuitry activity. However, the mechanistic understanding of how defective neural circuitry can induce neurogenesis defects in depression remains unclear. This review highlights the current findings supporting the neural circuitry-regulated neurogenesis, especially focusing on hippocampal neurogenesis regulated by the entorhinal cortex, with regard to memory, pattern separation, and mood. Taken together, these findings may pave the way for future progress in neural circuitry–neurogenesis coupling studies of depression.
format Online
Article
Text
id pubmed-7957816
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-79578162021-03-16 Neural Circuitry–Neurogenesis Coupling Model of Depression Kim, Il Bin Park, Seon-Cheol Int J Mol Sci Review Depression is characterized by the disruption of both neural circuitry and neurogenesis. Defects in hippocampal activity and volume, indicative of reduced neurogenesis, are associated with depression-related behaviors in both humans and animals. Neurogenesis in adulthood is considered an activity-dependent process; therefore, hippocampal neurogenesis defects in depression can be a result of defective neural circuitry activity. However, the mechanistic understanding of how defective neural circuitry can induce neurogenesis defects in depression remains unclear. This review highlights the current findings supporting the neural circuitry-regulated neurogenesis, especially focusing on hippocampal neurogenesis regulated by the entorhinal cortex, with regard to memory, pattern separation, and mood. Taken together, these findings may pave the way for future progress in neural circuitry–neurogenesis coupling studies of depression. MDPI 2021-02-28 /pmc/articles/PMC7957816/ /pubmed/33671109 http://dx.doi.org/10.3390/ijms22052468 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kim, Il Bin
Park, Seon-Cheol
Neural Circuitry–Neurogenesis Coupling Model of Depression
title Neural Circuitry–Neurogenesis Coupling Model of Depression
title_full Neural Circuitry–Neurogenesis Coupling Model of Depression
title_fullStr Neural Circuitry–Neurogenesis Coupling Model of Depression
title_full_unstemmed Neural Circuitry–Neurogenesis Coupling Model of Depression
title_short Neural Circuitry–Neurogenesis Coupling Model of Depression
title_sort neural circuitry–neurogenesis coupling model of depression
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957816/
https://www.ncbi.nlm.nih.gov/pubmed/33671109
http://dx.doi.org/10.3390/ijms22052468
work_keys_str_mv AT kimilbin neuralcircuitryneurogenesiscouplingmodelofdepression
AT parkseoncheol neuralcircuitryneurogenesiscouplingmodelofdepression