Nicotine increases cytosolic Ca2+ in vasopressin neurons

被引:13
作者
Shioda, S [1 ]
Yada, T
Muroya, S
Takigawa, M
Nakai, Y
机构
[1] Showa Univ, Sch Med, Dept Anat, Tokyo 142, Japan
[2] Kagoshima Univ, Sch Med, Dept Physiol, Kagoshima 890, Japan
[3] Kagoshima Univ, Sch Med, Dept Psychiat, Kagoshima 890, Japan
[4] Natl Inst Physiol Sci, Lab Intracellular Metab, Okazaki, Aichi 444, Japan
关键词
nicotine; acetylcholine receptor; vasopressin; cytosolic Ca2+; in vivo study; rat; cAMP;
D O I
10.1016/S0168-0102(97)00103-X
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Strong immunoreactivity for neuronal nicotinic acetylcholine receptor alpha 4 subunit was detected in neurons of the supraoptic nucleus (SON). At the ultrastructural level, immunoreactivity for alpha 4 was detected in the post-synaptic membranes as well as in the cytoplasmic matrices in the magnocellular neurons. Nicotine (1-10 mu M) increased cytosolic Ca2+ concentrations ([Ca2+](i)) in isolated arginine-vasopressin (AVP)-containing neurons in the rat SON. Nicotine (10 mu M) was less potent in increasing [Ca2+](i) in AVP-containing neurons than noradrenaline (1 mu M), a known neurotransmitter in the SON. The nicotine-induced [Ca2+](i) increase in AVP-containing neurons was markedly reduced when pre-treated with a protein kinase A (PKA) blocker, H89 (40 mu M). These findings suggest that nicotine, a known neurotransmitter in the SON, activates AVP-containing neurons via nicotinic acetylcholine receptor which is linked to stimulation of cAMP-PKA-regulated Ca2+ signaling pathway. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:311 / 318
页数:8
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