| First Author | Han W | Year | 2002 |
| Journal | Biochem Biophys Res Commun | Volume | 299 |
| Issue | 2 | Pages | 299-304 |
| PubMed ID | 12437986 | Mgi Jnum | J:80455 |
| Mgi Id | MGI:2445890 | Doi | 10.1016/s0006-291x(02)02632-3 |
| Citation | Han W, et al. (2002) Altered cocaine effects in mice lacking Ca(v)2.3 (alpha(1E)) calcium channel. Biochem Biophys Res Commun 299(2):299-304 |
| abstractText | Much evidence indicates that calcium channel plays a role in cocaine-induced behavioral responses. We assessed the contributions of Ca(v)2.3 (alpha(1E)) calcium channel to cocaine effects using Ca(v)2.3 knockout mice (Ca(v)2.3-/-). Acute administration of cocaine enhanced the locomotor activity in wild-type mice (Ca(v)2.3+/+), but failed to produce any response in Ca(v)2.3-/- mice. Repeated exposure to cocaine induced the behavioral sensitization and conditioned place preference in both genotypes. Pretreatment with a D1-receptor antagonist, SCH23390, blocked the cocaine-induced place preference in Ca(v)2.3+/+ mice; however, it had no significant effect in Ca(v)2.3-/- mice. Microdialysis and RT-PCR analysis revealed that the levels of extracellular dopamine and dopamine D1 and D2 receptor mRNAs were not altered in Ca(v)2.3-/- mice. These data indicate that Ca(v)2.3 channel contributes to the locomotor-stimulating effect of cocaine, and the deletion of Ca(v)2.3 channel reveals the presence of a novel pathway leading to cocaine rewarding which is insensitive to D1 receptor antagonist. |
