Arbilla S, Kamal L, Langer S Z
Eur J Pharmacol. 1979 Aug 1;57(2-3):211-7. doi: 10.1016/0014-2999(79)90367-4.
The release of 3H-GABA evoked by exposure to 30 mM potassium during 1 min was found to calcium independent in the rat occipital cortex and calcium dependent in the substantia nigra. Exposure to either muscimol 1 microM or GABA 1 microM inhibited the potassium-evoked release of 3H-GABA from the substantia nigra but not from the occipital cortex. The inhibitory effect of muscimol 1 microM on the potassium-evoked release of 3H-GABA from the substantia nigra was significantly antagonized by picrotoxin 10 microM. Exposure to either 10 or 100 microM pricrotoxin alone did not affect the potassium-evoked release of 3H-GABA. These results are compatible with the presence of a negative feedback mechanism in bagaergic nerve terminals of the rat substantia nigra which is mediated by presynaptic GABA autoreceptors. In addition, these results emphasize the importance of the calcium-dependent nature of the release of the neurotransmitter for demonstrating the modulation of transmitter release through presynaptic receptors.
发现在大鼠枕叶皮质中,暴露于30 mM钾1分钟所诱发的3H - GABA释放不依赖于钙,而在黑质中则依赖于钙。暴露于1 microM的蝇蕈醇或1 microM的GABA可抑制黑质中钾诱发的3H - GABA释放,但对枕叶皮质无此作用。1 microM的蝇蕈醇对黑质中钾诱发的3H - GABA释放的抑制作用被10 microM的印防己毒素显著拮抗。单独暴露于10或100 microM的印防己毒素不影响钾诱发的3H - GABA释放。这些结果与大鼠黑质中γ - 氨基丁酸能神经末梢存在由突触前GABA自身受体介导的负反馈机制相一致。此外,这些结果强调了神经递质释放的钙依赖性对于通过突触前受体证明递质释放调节的重要性。