Loss of Dysbindin Implicates Synaptic Vesicle Replenishment Dysregulation as a Potential Pathogenic Mechanism in Schizophrenia-Reference-Cited by-同舟云学术

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Loss of Dysbindin Implicates Synaptic Vesicle Replenishment Dysregulation as a Potential Pathogenic Mechanism in Schizophrenia

Published:2021-01 Issue: Volume:452 Page:138-152
ISSN:0306-4522
Container-title:Neuroscience
language:en
Short-container-title:Neuroscience

Author:

Hu Han,Wang Xuefeng,Li Chao,Li Yang,Hao Junfeng,Zhou Yuanli,Yang Xiaopeng,Chen Peihua,Shen Xuefeng,Zhang Shuli

Funder

National Science Foundation of China

Chinese Academy of Sciences

Publisher

Elsevier BV

Subject

General Neuroscience

Reference50 articles.

1. What can research on schizophrenia tell us about the cognitive neuroscience of working memory?;Barch;Neuroscience,2006

2. Unmasking group III metabotropic glutamate autoreceptor function at excitatory synapses in the rat CNS;Billups;J Physiol,2005

3. Dysbindin (DTNBP1) variants are associated with hallucinations in schizophrenia;Cheah;Eur Psychiatr,2015

4. DTNBP1, a schizophrenia susceptibility gene, affects kinetics of transmitter release;Chen;J Cell Biol,2008

5. Glutamatergic synaptic dysregulation in schizophrenia: therapeutic implications;Coyle;Handb Exp Pharmacol,2012

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