PSD-93 up-regulates the synaptic activity of corticotropin-releasing hormone neurons in the paraventricular nucleus in depression.
Animals
Corticotropin-Releasing Hormone
/ metabolism
Depression
/ metabolism
Female
Guanylate Kinases
/ metabolism
Humans
Hypothalamo-Hypophyseal System
/ metabolism
Male
Membrane Proteins
/ metabolism
Mice
Mice, Inbred C57BL
Neurons
/ physiology
Paraventricular Hypothalamic Nucleus
/ metabolism
Pituitary-Adrenal System
/ metabolism
Synaptic Transmission
/ physiology
Tumor Suppressor Proteins
/ metabolism
Up-Regulation
Corticotropin-releasing hormone
Depression
PSD-93
Paraventricular nucleus
Synaptic regulation
Journal
Acta neuropathologica
ISSN: 1432-0533
Titre abrégé: Acta Neuropathol
Pays: Germany
ID NLM: 0412041
Informations de publication
Date de publication:
12 2021
12 2021
Historique:
received:
06
07
2021
accepted:
10
09
2021
revised:
07
09
2021
pubmed:
19
9
2021
medline:
23
2
2022
entrez:
18
9
2021
Statut:
ppublish
Résumé
Since the discovery of ketamine anti-depressant effects in last decade, it has effectively revitalized interest in investigating excitatory synapses hypothesis in the pathogenesis of depression. In the present study, we aimed to reveal the excitatory synaptic regulation of corticotropin-releasing hormone (CRH) neuron in the hypothalamus, which is the driving force in hypothalamic-pituitary-adrenal (HPA) axis regulation. This study constitutes the first observation of an increased density of PSD-93-CRH co-localized neurons in the hypothalamic paraventricular nucleus (PVN) of patients with major depression. PSD-93 overexpression in CRH neurons in the PVN induced depression-like behaviors in mice, accompanied by increased serum corticosterone level. PSD-93 knockdown relieved the depression-like phenotypes in a lipopolysaccharide (LPS)-induced depression model. Electrophysiological data showed that PSD-93 overexpression increased CRH neurons synaptic activity, while PSD-93 knockdown decreased CRH neurons synaptic activity. Furthermore, we found that LPS induced increased the release of glutamate from microglia to CRH neurons resulted in depression-like behaviors using fiber photometry recordings. Together, these results show that PSD-93 is involved in the pathogenesis of depression via increasing the synaptic activity of CRH neurons in the PVN, leading to the hyperactivity of the HPA axis that underlies depression-like behaviors.
Identifiants
pubmed: 34536123
doi: 10.1007/s00401-021-02371-7
pii: 10.1007/s00401-021-02371-7
doi:
Substances chimiques
Membrane Proteins
0
Tumor Suppressor Proteins
0
Corticotropin-Releasing Hormone
9015-71-8
DLG2 protein, human
EC 2.7.4.8
Dlg2 protein, mouse
EC 2.7.4.8
Guanylate Kinases
EC 2.7.4.8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1045-1064Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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