Roles of aspartate and glutamate in synaptic transmission in rabbit retina. II. Inner plexiform layer.
Roles of aspartate and glutamate in synaptic transmission in rabbit retina. II. Inner plexiform layer.
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天冬氨酸和谷氨酸在兔视网膜突触传递中的作用。
DOI：
10.1152/jn.1985.53.3.714
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发表时间：
1985
影响因子：
2.5
通讯作者：
Dowling,JE
中科院分区：
文献类型：
--
作者：
Bloomfield,SA;Dowling,JE
细胞内记录是从兔子的灌注、分离的视网膜眼杯中的无长突细胞和神经节细胞获得的。将假定的神经递质天冬氨酸、谷氨酸和它们的几种类似物添加到超融合液中，同时监测视网膜神经元的膜电位和光响应性。 L-天冬氨酸和L-谷氨酸对所研究的绝大多数无长突细胞和神经节细胞的活性均表现出兴奋作用。然而，这些药物有时会通过产生膜电位超极化和光诱发反应的阻断来抑制内部视网膜神经元的反应。无论哪种情况，天冬氨酸和谷氨酸的作用都是难以区分的。谷氨酸类似物红藻氨酸和使君子氨酸对无长突细胞和神经节细胞的反应产生强烈的兴奋作用，其浓度比天冬氨酸或谷氨酸获得类似效果所需的浓度低约200倍。天冬氨酸类似物 n-甲基 DL-天冬氨酸 (NMDLA) 也产生强烈的兴奋作用，但其效力比红藻氨酸或使君子酸大约低三倍。有一次，我们遇到了一种神经节细胞，它被红藻氨酸去极化，但被 NMDLA 超极化。谷氨酸拮抗剂α-谷氨酸甲酯和天冬氨酸拮抗剂α-氨基己二酸有效阻断无长突和神经节细胞的反应。然而，在任何一种细胞上，一种拮抗剂总是明显比另一种更有效。我们检查了谷氨酸类似物 2-氨基-4-磷酸丁酸 (APB) 对内部视网膜神经元反应的作用，发现它选择性地消除了内部视网膜中的所有“开启”活动。连同我们发现 APB 选择性消除双极细胞反应（参见参考文献 6），这些数据支持双极细胞促进无长突细胞和神经节细胞“开启”活动的假设。我们的数据表明天冬氨酸和谷氨酸是视网膜内层的兴奋性递质，可能是从内丛状层的双极细胞轴突末端释放的。
Intracellular recordings were obtained from amacrine and ganglion cells in the superfused, isolated retina-eyecup of the rabbit. The putative neurotransmitters aspartate, glutamate, and several of their analogues were added to the superfusate while the membrane potential and light-responsiveness of the retinal neurons were monitored. Both L-aspartate and L-glutamate displayed excitatory actions on the activity of the vast majority of amacrine and ganglion cells studied. However, these agents occasionally appeared to inhibit the responses of the inner retinal neurons by producing hyperpolarization of the membrane potential and blockage of the light-evoked responses. In either case, the effects of aspartate and glutamate were indistinguishable. The glutamate analogues kainate and quisqualate produced strong excitatory effects on the responses of amacrine and ganglion cells at concentrations some 200-fold less than those needed to obtain similar effects with aspartate or glutamate. The aspartate analogue, n-methyl DL-aspartate (NMDLA), also produced strong excitatory effects but was approximately three times less potent than kainate or quisqualate. On one occasion, we encountered a ganglion cell that was depolarized by kainate, but hyperpolarized by NMDLA. The glutamate antagonist alpha-methyl glutamate and the aspartate antagonist alpha-amino adipate effectively blocked the responses of amacrine and ganglion cells. However, on any one cell, one antagonist was always clearly more potent than the other. We examined the actions of the glutamate analogue 2-amino-4-phosphonobutyrate (APB) on the responses of inner retinal neurons and found that it selectively abolished all "on" activity in the inner retina. Together with our finding that APB selectively abolishes on-bipolar cell responses (see Ref. 6), these data support the hypothesis that on-bipolar cells subserve the "on" activity of amacrine and ganglion cells. Our data suggest that aspartate and glutamate are excitatory transmitters in the inner retina, possibly being released from bipolar cell axon terminals in the inner plexiform layer.