Effects of Ca2+ channel antagonists on striatal dopamine and DOPA release, studied by in vivo microdialysis
Effects of Ca2+ channel antagonists on striatal dopamine and DOPA release, studied by in vivo microdialysis
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通过体内微透析研究 Ca2 通道拮抗剂对纹状体多巴胺和多巴释放的影响
DOI：
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发表时间：
1998
影响因子：
7.3
通讯作者：
S. Kaneko
中科院分区：
文献类型：
--
作者：
M. Okada;K. Wada;Kazuhiro Kiryu;Yuko Kawata;K. Mizuno;T. Kondo;H. Tasaki;S. Kaneko
1为了阐明调节纹状体多巴胺及其前体3，4-二羟基苯丙氨酸（DOPA）释放的机制，我们确定了各种Ca 2+通道拮抗剂的作用，N-型Ca 2+通道拮抗剂ω-芋螺毒素GVIA，P-型Ca 2+通道拮抗剂ω-agatoxin IVA，和Q-型Ca 2+通道拮抗剂ω-芋螺毒素MVIIC，通过使用体内微透析，对纹状体多巴胺和多巴的基础和Ca 2 +-和K+-诱发释放的影响。2 ω-芋螺毒素GVIA强烈抑制纹状体基础多巴胺释放（IC 50 =0.48 nM），而该毒素仅微弱调节纹状体基础多巴释放（IC 50 =9.55 nM）。 无论是ω-agatoxin IVA还是ω-conotoxin MVIIC都不影响多巴胺和多巴的基底纹状体释放。3 ω-芋螺毒素GVIA强烈抑制Ca 2 +-诱发的纹状体多巴胺释放（IC 50 =0.40 nM），而Ca 2 +-诱发的纹状体多巴释放仅被弱调节（IC 50 =10.51 nM）。 无论是ω-agatoxin IVA还是ω-conotoxin MVIIC都不会影响纹状体多巴胺和多巴的Ca 2 +-诱发释放。4 ω-agatoxin IVA和ω-conotoxin MVIIC均抑制K+诱发的纹状体多巴胺（ω-agatoxin IVA的IC 50 =2.65 nM; ω-conotoxin MVIIC的IC 50 =12.54 nM）和DOPA（ω-agatoxin IVA的IC 50 =0.15 nM; ω-conotoxin MVIIC的IC 50 =3.05 nM）释放，而ω-conotoxin GVIA对K+诱发的纹状体多巴胺和DOPA释放无影响。 5细胞外Ca 2+和K+浓度的增加（Ca 2 +-和K+-诱发的刺激）不影响体内酪氨酸羟化酶活性。6这些发现表明，纹状体多巴释放是神经递质样的，与纹状体多巴胺能传递机制不同，纹状体多巴传递至少部分受电压敏感性Ca 2+通道调节。
1 To elucidate the mechanisms regulating the release of striatal dopamine and its precursor, 3,4‐dihydroxyphenylalanine (DOPA), we determined the effects of various Ca2+ channel antagonists, an N‐type Ca2+ channel antagonist, ω‐conotoxin GVIA, a P‐type Ca2+ channel antagonist, ω‐agatoxin IVA, and a Q‐type Ca2+ channel antagonist, ω‐conotoxin MVIIC, on the basal and Ca2+‐ and K+‐evoked release of striatal dopamine and DOPA, by use of in vivo microdialysis. 2 ω‐Conotoxin GVIA strongly inhibited striatal basal dopamine release (IC50=0.48 nM), whereas this toxin only weakly modulated basal striatal DOPA release (IC50=9.55 nM). Neither ω‐agatoxin IVA nor ω‐conotoxin MVIIC affected the basal striatal release of dopamine and DOPA. 3 ω‐Conotoxin GVIA strongly inhibited Ca2+‐evoked striatal dopamine release (IC50=0.40 nM), whereas Ca2+‐evoked striatal DOPA release only was weakly modulated (IC50=10.51 nM). Neither ω‐agatoxin IVA nor ω‐conotoxin MVIIC affected the Ca2+‐evoked release of striatal dopamine and DOPA. 4 Both ω‐agatoxin IVA and ω‐conotoxin MVIIC inhibited the K+‐evoked release of striatal dopamine (IC50 of ω‐agatoxin IVA=2.65 nM; IC50 of ω‐conotoxin MVIIC=12.54 nM) and DOPA (IC50 of ω‐agatoxin IVA=0.15 nM; IC50 of ω‐conotoxin MVIIC=3.05 nM), whereas ω‐conotoxin GVIA had no effect on the K+‐evoked release of striatal dopamine and DOPA. 5 An increase in the extracellular Ca2+ and K+ concentrations (Ca2+‐ and K+‐evoked stimulation) did not affect tyrosine hydroxylase activity in vivo. 6 These findings suggest that striatal DOPA release is neurotransmitter‐like and that, unlike the mechanisms of striatal dopaminergic transmission, this striatal DOPA transmission is at least partly regulated by voltage‐sensitive Ca2+ channels.
多种 Ca2 通道类型共存来调节突触体神经递质的释放。
DOI：
10.1073/pnas.90.20.9518
发表时间：
1993
影响因子：
11.1
作者：
Turner,TJ;Adams,ME;Dunlap,K
通讯作者：
Dunlap,K
影响因子：
56.9
作者：
WHEELER, DB;RANDALL, A;TSIEN, RW
通讯作者：
TSIEN, RW