Inhibition of glutamate release by presynaptic kappa 1-opioid receptors in the guinea pig dentate gyrus.
Inhibition of glutamate release by presynaptic kappa 1-opioid receptors in the guinea pig dentate gyrus.
复制标题
豚鼠齿状回突触前 kappa 1-阿片受体抑制谷氨酸释放。
DOI：
10.1152/jn.1994.72.4.1697
复制
发表时间：
1994
影响因子：
2.5
通讯作者：
Chavkin,C
中科院分区：
文献类型：
--
作者：
Simmons,ML;Terman,GW;Drake,CT;Chavkin,C
1. kappa 1-阿片受体的激活抑制豚鼠海马齿状回的兴奋性传递。目前的研究使用解剖学和生理学方法来区分这些受体的突触前和突触后定位。2. 单侧损伤内吸皮层，引起齿状分子层穿孔通路传入神经变性，用选择性激动剂标记kappa 1-阿片结合位点[3H]-U69593。与对侧分子层和假性病变对照相比，同侧病变齿状回分子层的结合密度显著降低。3. 配对脉冲促进是一种神经生理学范式，用于区分抑制兴奋性神经传递的药物的突触前和突触后作用位点。U69593降低了单种群峰值的幅度，增加了成对脉冲的促进度。当刺激强度增加以补偿兴奋性传递的抑制时，配对脉冲促进的增强得以维持。kappa 1受体激活的这些作用与突触前抑制兴奋性神经递质释放后的效果相似，支持了U69593突触前抑制齿状回兴奋性氨基酸释放的假设。4. 在齿状分子层通过压力喷射局部应用谷氨酸可诱发场兴奋性突触后电位，这与电刺激穿孔通路引起的电位相似。两种反应均对非n-甲基-d -天冬氨酸受体拮抗剂6-氰基-7-硝基喹啉-2,3-二酮敏感。U69593对穿孔通路刺激引起的反应有抑制作用，但对谷氨酸刺激引起的反应无影响。（摘要删节250字）
1. Activation of kappa 1-opioid receptors inhibits excitatory transmission in the hippocampal dentate gyrus of the guinea pig. The present studies used both anatomic and physiological approaches to distinguish between a pre- and postsynaptic localization of these receptors. 2. The entorhinal cortex was lesioned unilaterally to cause degeneration of perforant path afferents to the dentate molecular layer, and kappa 1-opioid binding sites were measured by labeling with the selective agonist, [3H]-U69593. Binding density was reduced significantly in the dentate gyrus molecular layer ipsilateral to the lesion compared with the contralateral molecular layer and with sham-lesioned controls. 3. Paired-pulse facilitation is a neurophysiologic paradigm that has been used to differentiate pre- and postsynaptic sites of action for agents that inhibit excitatory neurotransmission. U69593 reduced the amplitude of single population spikes and increased the degree of paired pulse facilitation. The potentiation of paired-pulse facilitation was maintained when the stimulation intensity was increased to compensate for the inhibition of excitatory transmission. These effects of kappa 1-receptor activation were similar to those seen after presynaptic inhibition of excitatory neurotransmitter release and support the hypothesis that U69593 presynaptically inhibits excitatory amino acid release in the dentate gyrus. 4. Local application of glutamate by pressure ejection in the dentate molecular layer evoked field excitatory postsynaptic potentials that mimicked those evoked by electrical stimulation of the perforant path. Both responses were sensitive to the non-N-methyl-D-aspartate glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione. U69593 inhibited responses evoked by perforant path stimulation but had no effect on responses evoked by glutamate application.(ABSTRACT TRUNCATED AT 250 WORDS)