Dysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments.

Details

Serval ID
serval:BIB_5F8C66EA0DF8
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Dysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments.
Journal
Molecular psychiatry
Author(s)
Petrelli F., Dallérac G., Pucci L., Calì C., Zehnder T., Sultan S., Lecca S., Chicca A., Ivanov A., Asensio C.S., Gundersen V., Toni N., Knott G.W., Magara F., Gertsch J., Kirchhoff F., Déglon N., Giros B., Edwards R.H., Mothet J.P., Bezzi P.
ISSN
1476-5578 (Electronic)
ISSN-L
1359-4184
Publication state
Published
Issued date
04/2020
Peer-reviewed
Oui
Volume
25
Number
4
Pages
732-749
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
Astrocytes orchestrate neural development by powerfully coordinating synapse formation and function and, as such, may be critically involved in the pathogenesis of neurodevelopmental abnormalities and cognitive deficits commonly observed in psychiatric disorders. Here, we report the identification of a subset of cortical astrocytes that are competent for regulating dopamine (DA) homeostasis during postnatal development of the prefrontal cortex (PFC), allowing for optimal DA-mediated maturation of excitatory circuits. Such control of DA homeostasis occurs through the coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) together with organic cation transporter 3 and monoamine oxidase type B, two key proteins for DA uptake and metabolism. Conditional deletion of VMAT2 in astrocytes postnatally produces loss of PFC DA homeostasis, leading to defective synaptic transmission and plasticity as well as impaired executive functions. Our findings show a novel role for PFC astrocytes in the DA modulation of cognitive performances with relevance to psychiatric disorders.
Pubmed
Web of science
Open Access
Yes
Create date
29/08/2018 15:09
Last modification date
19/06/2020 6:21
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