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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Characterization of electrically evoked (3H)-D-aspartate release from hippocampal slices.
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Characterization of electrically evoked (3H)-D-aspartate release from hippocampal slices.

机译：从海马切片电诱发的（3H）-D-天冬氨酸释放的表征。

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Electrical stimulation has certain advantages over chemical stimulation methods for the study of neurotransmitter release in brain slices. However, measuring detectable quantities of electrically evoked release of endogenous or radiolabeled markers of excitatory amino acid neurotransmitters has required current intensities or frequencies much higher than those usually required to study other transmitter systems. We demonstrate here that [3H]-D-aspartate (D-ASP) release can be detected from hippocampal slices at lower stimulation intensities in the presence of a glutamate reuptake inhibitor. Subsequently, we optimized the electrical stimulus parameters for characterizing electrically evoked D-ASP release. Under the experimental conditions described, greater than 90% of electrically evoked D-ASP release is calcium-dependent. Evoked D-ASP release is markedly reduced by pre-treating slices with the synaptic vesicle toxin bafilomycin A1 (BAF A1) or in the presence of 10-mM magnesium. Evoked D-ASP release is also reduced to variable degrees by N- and P/Q type voltage-sensitive calcium channel antagonists. Neither spontaneous efflux nor evoked D-ASP release were affected by NMDA, AMPA or group I metabotropic glutamate receptor (mGluR) antagonists. Evoked D-ASP release was reduced in the presence of an adenosine A1 receptor agonist and potentiated by treatment with a group I mGluR5 agonist. Evoked [3H]-D-ASP release was similar in magnitude to evoked [3H]-L-glutamate (L-GLU) release. Finally, in separate experiments using the same electrical stimulus parameters, more than 90% of electrically evoked endogenous L-GLU release was calcium dependent, a pattern similar to that observed for evoked [3H]-D-ASP release. Taken together, these results indicate that electrically evoked [3H]-D-ASP release mimics evoked glutamate release in brain slices under the experimental conditions employed in these studies.
机译：在研究脑片中神经递质的释放方面，电刺激优于化学刺激方法。然而，测量兴奋性氨基酸神经递质的内源性或放射性标记的标记物的电诱发释放的可检测量所需的电流强度或频率远高于研究其他传输器系统通常所需的电流强度或频率。我们在这里证明，可以在谷氨酸再摄取抑制剂的存在下以较低的刺激强度从海马切片中检测到[3H] -D-天冬氨酸（D-ASP）释放。随后，我们优化了电刺激参数，以表征电诱发的D-ASP释放。在所述的实验条件下，超过90％的电诱发D-ASP释放是钙依赖性的。通过用突触小囊毒素bafilomycin A1（BAF A1）或在存在10mM镁的情况下预处理切片，可显着降低诱发的D-ASP释放。 N-和P / Q型电压敏感钙通道拮抗剂还可以将D-ASP诱发的释放程度降低。 NMDA，AMPA或I组代谢型谷氨酸受体（mGluR）拮抗剂均不影响自发外流或诱发D-ASP释放。在存在腺苷A1受体激动剂的情况下，诱发的D-ASP释放降低，并通过用I组mGluR5激动剂治疗而增强。诱发的[3H] -D-ASP释放的程度与诱发的[3H] -L-谷氨酸（L-GLU）释放相似。最后，在使用相同电刺激参数的单独实验中，超过90％的电诱发内源性L-GLU释放是钙依赖性的，该模式类似于诱发的[3H] -D-ASP释放。两者合计，这些结果表明，在这些研究中使用的实验条件下，电诱发的[3H] -D-ASP释放模拟脑切片中诱发的谷氨酸释放。

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