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In vivo CRF release in rat amygdala is increased during cocaine withdrawal in self‐administering rats
Author(s) -
Richter Regina M.,
Weiss Friedbert
Publication year - 1999
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(19990615)32:4<254::aid-syn2>3.0.co;2-h
Subject(s) - anxiogenic , amygdala , microdialysis , drug withdrawal , self administration , kindling , psychology , central nucleus of the amygdala , endocrinology , medicine , anesthesia , pharmacology , neuroscience , central nervous system , drug , receptor , anxiolytic , stimulation
Previous studies have suggested a role for corticotropin‐releasing factor (CRF) in the central nucleus of the amygdala (CeA) in the aversive and anxiogenic effects of withdrawal from opiates and ethanol. To test whether this role of CRF extends to cocaine withdrawal as well, the release of CRF in rat amygdala was monitored by intracranial microdialysis during a 12‐hour session of intravenous cocaine self‐administration and subsequent 12‐hour cocaine withdrawal period. Cocaine self‐administration tended to lower dialysate CRF concentrations to approximately 75% of CRF levels in controls. In contrast, subsequent cocaine withdrawal produced a profound increase in CRF release, which reached peak levels of approximately 400% of baseline between 11 and 12 hours post‐cocaine. These results provide evidence that cocaine withdrawal activates CRF neurons in the amygdala, a site that has been implicated in emotional and anxiogenic effects of stress and drug withdrawal syndromes. Synapse 32:254–261, 1999. © 1999 Wiley‐Liss, Inc.