| Co-Investigator(Kenkyū-buntansha) |
MICHIKAWA Takayuki The University of Tokyo, Inst.Medical Science, Research Associate, 医科学研究所, 助手 (90282516)
FURUICHI Teiichi The University of Tokyo, Inst.Medical Science, Assosiate Prof., 医科学研究所, 助教授 (50219094)
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| Research Abstract |
The inositol 1,4,5-triaphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R(IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion in internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore assisted laser inactivation resulted in growth cones arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.
Changes in [Ca2+]i are an essential factor regulating egg activation. Matured ascidian eggs are arrested at metaphase I , and two series of [Ca2+]i transients have been observed after fertilization : Ca2+ waves just fertilization (Series I) and [Ca2+]i oscillation between the first and second polar body extrusion (Series II). We investigated mechanisms involved in the elevation of [Ca2+]i and the role of the [Ca2+]i transients during egg activation in Ciona savignyi. The monoclonal antibody 18A10 against IP3 receptor type 1, which inhibits IP3-induced Ca2+ release in hamster and mouse eggs, did not show substantial inhibitory effects on series I or egg deformation, whereas Series II and the first cell division were inhibited by the antibody. Ruthenium red, an inhibitor of ryanodine receptor-mediated Ca2+ release, had no apparent effect of [Ca2+]i transients and other events related to the egg activation.
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