Prevention and reversal of social stress-escalated cocaine self-administration in mice by intra-VTA CRFR1 antagonism

Prevention and reversal of social stress-escalated cocaine self-administration in mice by... Psychopharmacology (2017) 234:2813–2821 DOI 10.1007/s00213-017-4676-8 ORIGINAL INVESTIGATION Prevention and reversal of social stress-escalated cocaine self-administration in mice by intra-VTA CRFR1 antagonism 1,2 1 1,3 Xiao Han & Joseph F. DeBold & Klaus A. Miczek Received: 8 November 2016 /Accepted: 16 June 2017 /Published online: 11 July 2017 Springer-Verlag GmbH Germany 2017 Abstract Intra-VTA antagonism of CRFR1 was sufficient to reverse Background A history of brief intermittent social defeat stress social defeat stress-escalated cocaine self-administration. can escalate cocaine self-administration and induce long-term Conclusion These findings suggest that CRF and CRFR1 ex- adaptations in the mesolimbic dopamine system. Extra- ert multiple roles in the response to social stress that are rele- hypothalamic corticotrophin releasing factor (CRF) has been vant to escalated cocaine self-administration. shown to be closely associated with stress-induced escalation . . of drug use. How repeated stress modulates CRF release in the Keywords Social defeat stress CRF microdialysis . . ventral tegmental area (VTA) and the roles of CRF receptors CRFR1 Intravenous cocaine self-administration . . during different phases of stress-induced cocaine self- Microinjection VTA Mice administration remain to be defined. Objective The current study examines the roles of CRF and CRF receptor 1 (CRFR1) in escalated intravenous cocaine http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Psychopharmacology Springer Journals

Prevention and reversal of social stress-escalated cocaine self-administration in mice by intra-VTA CRFR1 antagonism

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany
Subject
Biomedicine; Neurosciences; Pharmacology/Toxicology; Psychiatry
ISSN
0033-3158
eISSN
1432-2072
D.O.I.
10.1007/s00213-017-4676-8
Publisher site
See Article on Publisher Site

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