Ca2+ imaging of urinary bladder myocyte from voltage dependent Ca2+ channel β3 subunit deficient mouse

• Published in: Journal of Pharmacological Sciences 2003, Vol.91 (suppl.2), p.243-243
• Main Authors: Kozo Morimura, Manabu Murakami, Hisao Yamamura, Susumu Ohya, Katsuhiko Muraki, Kazuo Nunoki, Teruyuki Yanagisawa, Yuji Imaizumi
• Format: Article
• Language: Japanese
• ISSN: 1347-8613

Auxiliary β subunits of voltage dependent Ca2+ channels (VDCC) are known to modify VDCC functions of α 1 subunit. Among β subunits, β3 is abundantly expressed in smooth muscle cells (SMC). To elucidate physiological roles of β3 subunits in Ca2+ mobilization in SMCs, Ca2+ images of urinary bladder SMCs (UBSMC) from VDCC β3 null mice (β3-/-) were analyzed under voltage clamp. In resting conditions, local Ca2+ transients, Ca2+ sparks, occurred spontaneously mainly in peripheral areas in UBSMCs and activated Ca2+ activated K+ channels to elicit spontaneous transient outward currents (STOCs). Neither amplitude nor frequency of STOCs was altered in β3-/-. During depolarization, early Ca2+ transients (Ca2+ hotspot) were observed in peripheral areas and spread into other areas of myocytes. Ca2+ current density was significantly reduced in β3-/-. The increase in [Ca2+]i in hotspots at 30 ms from the start of depolarization was significantly smaller in β3-/-. Moreover, the number of hotspots tended to be decreased in β3-/-. These results indicate that Ca2+ events to induce excitation-contraction coupling were less functional in β3-/- UBSMCs presumably because of the deficiency of VDCC function but Ca2+ sparks were not affected.