| First Author | Murakami M | Year | 2007 |
| Journal | Brain Res | Volume | 1160 |
| Pages | 102-12 | PubMed ID | 17588550 |
| Mgi Jnum | J:123326 | Mgi Id | MGI:3717990 |
| Doi | 10.1016/j.brainres.2007.05.041 | Citation | Murakami M, et al. (2007) Modified behavioral characteristics following ablation of the voltage-dependent calcium channel beta3 subunit. Brain Res 1160:102-12 |
| abstractText | Voltage-dependent calcium channels are important for calcium influx and the ensuing intracellular calcium signal in various excitable membranes. The beta subunits of these channels modify calcium currents through pore-forming alpha1 subunits of the high-voltage- activated calcium channels. In the present study, beta3 subunit-null mice were used to investigate the importance of the beta3 subunit of the voltage-dependent calcium channel, which couples with the CaV2.2 (alpha1B) subunit to form the major component of neuronal N-type calcium channels in the brain. Western blot analysis revealed a significant decrease in N-type calcium channels in beta3 subunit-null mice, while protein levels of other high-voltage-activated calcium channel alpha1 subunits were unchanged. Immunoprecipitation analysis with an anti-CaV2.2 antibody showed that reshuffling of the assembly of N-type channels had occurred in the beta3 subunit-null mice. Ablation of this subunit resulted in modified nociception, decreased anxiety, and increased aggression. The beta3 subunit-null mice also showed impaired learning ability. These results suggest the importance of voltage-dependent calcium channels and the key role of the beta3 subunit in memory formation, nociceptive sensory transduction, and various neurological signal transduction pathways. |
