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ω-芋螺毒素GVIA与海马去甲肾上腺素释放的药理学调节

Omega-conotoxin GVIA and pharmacological modulation of hippocampal noradrenaline release.

作者信息

Dooley D J, Lupp A, Hertting G, Osswald H

机构信息

Gödecke Research Institute, Freiburg, F.R.G.

出版信息

Eur J Pharmacol. 1988 Mar 29;148(2):261-7. doi: 10.1016/0014-2999(88)90572-9.

Abstract

The tritium overflow evoked by electrical stimulation of rabbit hippocampal slices labeled with [3H]noradrenaline was inhibited by omega-conotoxin GVIA, a peptide modulator of the N-type voltage-sensitive calcium channel (N-VSCC). The magnitude of this inhibition was unchanged in the presence of substances which interact with N- and/or L-VSCCs (cadmium, neomycin, (-)- and (+)-202-791), alpha 2-adrenoceptors (idazoxan, UK-14304), protein kinase C (4 beta-phorbol-12,13-dibutyrate) or potassium channels (4-aminopyridine). This finding suggests that the attenuation of calcium-dependent neurotransmitter release by omega-conotoxin GVIA is relatively insensitive to alterations of such release effected by other substances.

摘要

用[3H]去甲肾上腺素标记的兔海马切片经电刺激诱发的氚溢出,被ω-芋螺毒素GVIA抑制,ω-芋螺毒素GVIA是N型电压敏感性钙通道(N-VSCC)的一种肽调节剂。在存在与N型和/或L型电压敏感性钙通道相互作用的物质(镉、新霉素、(-)-和(+)-202-791)、α2-肾上腺素能受体(咪唑克生、UK-14304)、蛋白激酶C(4β-佛波醇-12,13-二丁酸酯)或钾通道(4-氨基吡啶)时,这种抑制的程度没有改变。这一发现表明,ω-芋螺毒素GVIA对钙依赖性神经递质释放的减弱对其他物质引起的这种释放改变相对不敏感。

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