Thate A, Meyer D K
Pharmakologisches Institut, Universität Freiburg, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1989 Mar;339(3):359-61. doi: 10.1007/BF00173592.
omega-Conotoxin GVIA (omega-CT) diminished the potassium-induced in vitro release of 3H-gamma-aminobutyric acid (3H-GABA) from slices of rat neostriatum in a manner which depended on the concentration of potassium. omega-CT (0.1 mmol/l) decreased the release of 3H-GABA induced by 25 mmol/l K+ from 11.6% to 6.1% of tissue content, ie. by 48%, while it did not affect the release of 3H-GABA caused by 20 mmol/l K+, which was 4.8% of tissue content. However, in the presence of a polyclonal antiserum or cysteamine (600 mumol/l), both of which diminish the effects of endogenous somatostatin, 0.1-10 nmol/l omega-CT decreased the release of 3H-GABA induced by 20 mmoles/l K+ by 40%. It is concluded that omega-CT did not only inhibit GABA-neurones, but had an additional inhibitory effect on somatostatin neurones which are known to depress the release of 3H-GABA. It is further concluded that neuronal interactions, which are possible in brain slice preparations, may impede the interpretation of effects of drugs, especially if agents are used which affect basic mechanisms of transmitter release and thus the release of various transmitters from neurones.
ω-芋螺毒素GVIA（ω-CT）能以一种依赖于钾离子浓度的方式，减少钾离子诱导的大鼠新纹状体切片中3H-γ-氨基丁酸（3H-GABA）的体外释放。ω-CT（0.1 mmol/l）可使25 mmol/l K+诱导的3H-GABA释放量从组织含量的11.6%降至6.1%，即降低了48%，而它对20 mmol/l K+诱导的3H-GABA释放（占组织含量的4.8%）没有影响。然而，在存在多克隆抗血清或半胱胺（600 μmol/l）的情况下，这两种物质都会减弱内源性生长抑素的作用，0.1 - 10 nmol/l的ω-CT可使20 mmol/l K+诱导的3H-GABA释放量降低40%。结论是，ω-CT不仅抑制GABA能神经元，而且对已知可抑制3H-GABA释放的生长抑素能神经元有额外的抑制作用。进一步的结论是，在脑片制备中可能存在的神经元相互作用，可能会妨碍对药物作用的解释，特别是如果使用了影响递质释放基本机制从而影响神经元释放各种递质的药物。
