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Exp Neurobiol 2013; 22(3): 224-231
Published online September 30, 2013
https://doi.org/10.5607/en.2013.22.3.224
© The Korean Society for Brain and Neural Sciences
Eun-Sol Jung, Hyo Jin Lee, Hye-Ri Sim and Ja-Hyun Baik*
Molecular Neurobiology Laboratory, College of Life Sciences and Biotechnology, Department of Life Sciences, Korea University, Seoul 136-701, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-3290-3455, FAX: 82-2-927-9028
e-mail: jahyunb@korea.ac.kr
To determine the role of dopamine D2 receptor (D2R) in the nucleus accumbens (NAc) core in cocaine-induced behavioral sensitization, D2R antagonist, raclopride was bilaterally microinjected (2.5 or 5 nmol) into the NAc core of WT and D2R-/- mice and the initiation and expression phase of cocaine-mediated locomotor sensitization were analyzed. WT and D2R knockout (D2R-/-) mice received bilateral injections of either saline, or raclopride at the NAc core 30 min before each of five daily repeated injections of saline or cocaine (15 mg/kg i.p.). Following 2 weeks of withdrawal after repeated exposure to cocaine, the animals were pre-treated with an intra-accumbal injection of vehicle or raclopride before receiving a systemic cocaine challenge for the expression of sensitization. Animals which had been microinjected raclopride into NAc core displayed the enhancement of cocaine-induced behavioral response for the initiation but also for the expression of sensitization in WT as well as in D2R-/- mice, which was thus unaltered as compared to vehicle-injected control group. These results suggest that D2R in NAc core is not involved in cocaine-induced behavioral sensitization.
Keywords: dopamine receptor, nucleus accumbens, cocaine, addiction, behavioral sensitization