Project/Area Number |
10680708
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | Showa University |
Principal Investigator |
SHIODA Seiji Showa University School of Medicine, Professor, 医学部, 教授 (80102375)
|
Co-Investigator(Kenkyū-buntansha) |
YAGI Takashi National Inst. Physiol. Sci., Associate Professor, 生理学研究所, 教授 (10241241)
YADA Toshihiko Kagoshima University School of Medicine, Associate Professor, 医学部, 助教授 (60166527)
NAKAJO Shigeo Showa University School of Pharm., Associate Professor, 薬学部, 助教授 (50119236)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
|
Keywords | PACAP / Noradrenalin / Vasopressin / Siganal transduction / Calcium channel / Neuroendocrine cells / Hypothalamus |
Research Abstract |
PACAP-containing axon terminals innervate arginine-vasopressin (AVP)-containing neurons in the rat hypothalamic supraoptic nucleus (SON). PACAP receptor (PACAPR) mRNA was expressed at high-levels in SON expressed in AVP-containing neurons. Although the pathway arising from PACAP/NA (noradrenalin)-containing neurons in the ventrolateral medulla is involved in the regulation of AVP, the precise mechanism of action and physiological significance of the coexistence of PACAP and NA still need to be investigated. Both PACAP and NA induced large increases in the [Ca2+]I in isolated AVP-containing neurons. When PACAP and NA were added together, they evoked larger increase in [Ca2+]I in AVP neurons. An inhibitor of PKA completely inhibited the PACAP-induced increase in [Ca2+]I, and partly the NA-induced increase in AVP-containing neurons. We found that T-type calcium channels might contribute to Ca2+ influx during action potentials through cAMP-PKA signaling pathway and L-type currents might contribute to the generation of bursting activity. PACAP and NA, co-released from the same axon terminals, may act synergistically to stimulate calcium signaling in AVP neurons, which is mediated by both cAMP-PKA pathway and L-type Ca2+ channel. PACAP/NA may regulate the functions of AVP-containing neurons which participate in the control of plasma osmolarity and blood pressure.
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