Ventral Tegmental Area BDNF Induces an Opiate-Dependent–Like Reward State in Naïve Rats-Reference-Cited by-同舟云学术

Ventral Tegmental Area BDNF Induces an Opiate-Dependent–Like Reward State in Naïve Rats

Published:2009-06-26 Issue:5935 Volume:324 Page:1732-1734
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Vargas-Perez Hector¹,Ting-A-Kee Ryan²,Walton Christine H.³,Hansen D. Micah³,Razavi Rozita¹,Clarke Laura²,Bufalino Mary Rose²,Allison David W.³,Steffensen Scott C.³,van der Kooy Derek¹²

Affiliation:

1. Department of Molecular Genetics, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada.

2. Institute of Medical Science, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada.

3. Department of Psychology, Brigham Young University, Provo, UT 84602, USA.

Abstract

BDNF and Drug Dependence Brain-derived neurotrophic factor (BDNF) is a growth factor involved in neuronal plasticity that is expressed after chronic administration of drugs of abuse and may play a crucial role in chronic opiate effects. Vargas-Perez et al. (p. 1732 , published online 28 May) found that BDNF was directly involved in the switching mechanism in the ventral tegmental area, from an opiate-naïve, dopamine-independent drug reward substrate to an opiate-dependent, dopamine-dependent motivational substrate. In the ventral tegmental area, BDNF changed the action of GABA-A receptors from inhibitory to excitatory. This change led to behavioral changes that defined a neurobiological boundary between the acute phase of drug-taking and addiction.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference20 articles.

1. GABAAreceptors in the ventral tegmental area control bidirectional reward signalling between dopaminergic and non-dopaminergic neural motivational systems

2. Opiate state controls bi-directional reward signaling via GABAA receptors in the ventral tegmental area

3. Motivational state determines the functional role of the mesolimbic dopamine system in the mediation of opiate reward processes

4. BDNF-induced TrkB activation down-regulates the K+–Cl− cotransporter KCC2 and impairs neuronal Cl− extrusion

5. BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain

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