Contestabile A, Migani P, Poli A, Villani L, Barnabei O
Brain Res. 1983 Mar 7;262(2):339-43. doi: 10.1016/0006-8993(83)91030-2.
Inhibition of GABA transaminase which led to a several-fold increase of GABA levels in the goldfish optic tectum or diazepam pre-treatment, were unable to protect tectal neurons from kainic acid neurotoxicity, as judged by light and electron microscopic observations and by the drop of marker enzymes for neurotransmitters. In an in vitro preparation of tectal slices GABA, added to the incubation medium, had no effect on a metabolic parameter (CO2 production from exogenous glucose) related to the excitatory action of kainic acid. It is concluded that, in the goldfish optic tectum, pharmacological manipulation cannot enhance the activity of GABAergic circuits to the extent necessary to block the neuroexcitatory and neurotoxic action of kainic acid.
通过光镜和电镜观察以及神经递质标记酶的下降情况判断，抑制金鱼视顶盖中的γ-氨基丁酸转氨酶（这会导致视顶盖中γ-氨基丁酸水平增加数倍）或地西泮预处理，均无法保护顶盖神经元免受红藻氨酸的神经毒性作用。在视顶盖切片的体外制备中，添加到孵育培养基中的γ-氨基丁酸，对与红藻氨酸兴奋作用相关的代谢参数（外源性葡萄糖产生二氧化碳）没有影响。得出的结论是，在金鱼视顶盖中，药物操作无法将γ-氨基丁酸能回路的活性增强到阻断红藻氨酸神经兴奋和神经毒性作用所需的程度。
