Selective Inactivation of the Ventral Hippocampus Attenuates Cue-induced and Cocaine-primed Reinstatement of Drug-seeking in Rats

Overview

Journal Neurobiol Learn Mem

Specialties Biology
Neurology
Social Sciences

Date 2007 Mar 6

PMID 17337218

Citations 72

Authors

Jason L Rogers

Ronald E See

Affiliations

Soon will be listed here.

Abstract

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 (B/M; 1.0 mM/0.1 mM) [corrected] 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.

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