Absence of the neurogenesis-dependent nuclear receptor TLX induces inflammation in the hippocampus.
DCX
Hippocampus
Interleukin-1β
Microglia
Neurogenesis
TLX
Journal
Journal of neuroimmunology
ISSN: 1872-8421
Titre abrégé: J Neuroimmunol
Pays: Netherlands
ID NLM: 8109498
Informations de publication
Date de publication:
15 06 2019
15 06 2019
Historique:
received:
19
05
2017
revised:
18
08
2017
accepted:
18
08
2017
pubmed:
29
8
2017
medline:
24
3
2020
entrez:
29
8
2017
Statut:
ppublish
Résumé
The orphan nuclear receptor TLX (Nr2e1) is a key regulator of hippocampal neurogenesis. Impaired adult hippocampal neurogenesis has been reported in neurodegenerative and psychiatric conditions including dementia and stress-related depression. Neuroinflammation is also implicated in the neuropathology of these disorders, and has been shown to negatively affect hippocampal neurogenesis. To investigate a role for TLX in hippocampal neuroinflammation, we assessed microglial activation in the hippocampus of mice with a spontaneous deletion of TLX. Results from our study suggest that a lack of TLX is implicated in deregulation of microglial phenotype and that consequently, the survival and function of newborn cells in the hippocampus is impaired. TLX may be an important target in understanding inflammatory-associated impairments in neurogenesis.
Identifiants
pubmed: 28844503
pii: S0165-5728(17)30204-7
doi: 10.1016/j.jneuroim.2017.08.008
pii:
doi:
Substances chimiques
Dcx protein, mouse
0
Doublecortin Protein
0
IL1B protein, mouse
0
Interleukin-1beta
0
Nr2e1 protein, mouse
0
Receptors, Cytoplasmic and Nuclear
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
87-96Informations de copyright
Copyright © 2017 Elsevier B.V. All rights reserved.