Abstract：
: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.
journal_name
Brain Resjournal_title
Brain researchauthors
Murakami M,Nakagawasai O,Yanai K,Nunoki K,Tan-No K,Tadano T,Iijima Tdoi
10.1016/j.brainres.2007.05.041subject
Has Abstractpub_date
2007-07-30 00:00:00pages
102-12eissn
0006-8993issn
1872-6240pii
S0006-8993(07)01247-4journal_volume
1160pub_type
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