Journal
NEUROBIOLOGY OF LEARNING AND MEMORY
Volume 87, Issue 4, Pages 688-692Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nlm.2007.01.003
Keywords
cocaine; hippocampus; reinstatement; relapse; self-administration
Funding
- NCRR NIH HHS [C 06 RR015455, C06 RR015455] Funding Source: Medline
- NIDA NIH HHS [DA015369, R01 DA010462, P50 DA015369, R01 DA010462-09, DA010462] Funding Source: Medline
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Recent evidence suggests that the hippocampus may have a functional role in mediating relapse to cocaine-seeking behavior. Based on the importance of the ventral CA subfields in mediating reward, the present experiment determined the effects of temporary inactivation of the ventral hippocampus on reinstatement of cocaine-seeking in a rodent model of relapse. Male, Sprague-Dawley rats self-administered i.v. cocaine (0.6 mg/kg/infusion) in the presence of discrete conditioned cues (tone + light) in daily 2-h sessions for ten days. Following seven days of extinction sessions in which neither cues nor drug were available, rats underwent four reinstatement tests in a counterbalanced, within-subjects design. Bilateral microinjections of GABA receptor agonists (baclofen/muscimol-0.1/1.0 mM) into the ventral hippocampus significantly attenuated cue-induced and cocaine-primed reinstatement compared with vehicle microinjections in the same rats. In contrast, injections just outside the ventral hippocampus did not block either form of reinstatement. Furthermore, inactivation failed to affect responding for food reinforcement, baseline extinction responding, or locomotor activity. These data indicate that the ventral hippocampus plays an important role in the relapse to cocaine-seeking behavior and may interact with key limbic structures previously implicated in cocaine addiction. (C) 2007 Elsevier Inc. All rights reserved.
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