DBI/ACBP loss-of-function does not affect anxiety-like behaviour but reduces anxiolytic responses to diazepam in mice
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- 作者：Lionel Budrya ; b ; Khalil Bouyakdana ; c ; Stephanie Tobina ; b ; Demetra Rodarosa ; Ann-Britt Marcherf ; Susanne Mandrupf ; Stephanie Fultona ; d ; Thierry Alquiera ; b ; c ; e ; thierry.alquier@umontreal.ca" class="auth_mail" title="E-mail the corresponding author
- 关键词：ACBP ; acyl-CoA binding protein ; DBI ; diazepam binding inhibitor ; GABA ; gamma-aminobutyric acid ; CBR ; central benzodiazepine receptor ; PBR ; peripheral benzodiazepine receptor ; CNS ; central nervous system ; GFAP ; glial fibrillary acidic protein ; ICV ; intracerebroventricular ; ODN ; octadecaneuropeptide ; TTN ; triakontatetraneuropeptide ; NAM ; negative allosteric modulator ; PAM ; positive allosteric modulator ; SVZ ; subventricular zone ; nRT ; thalamic reticular nucleus ; PVN ; paraventricular nucleus ; EPM ; e
- 刊名：Behavioural Brain Research
- 出版年：2016
- 出版时间：15 October 2016
- 年：2016
- 卷：313
- 期：Complete
- 页码：201-207
- 全文大小：1812 K
文摘
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ACBP deficiency in GFAP astrocytes does not affect anxiety-like behaviour.
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Anxiety is not affected in whole body ACBP knock-out mice.
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Whole body ACBP knock-out mice have impaired anxiolytic responses to diazepam.