首页> 美国卫生研究院文献>The Journal of Physiology >Responses mediated by excitatory amino acid receptors in solitary retinal ganglion cells from rat.
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Responses mediated by excitatory amino acid receptors in solitary retinal ganglion cells from rat.

机译:大鼠离体视网膜神经节细胞中兴奋性氨基酸受体介导的反应。

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摘要

1. The pharmacological properties of excitatory amino acid responses on ganglion cells dissociated from the rat retina were examined with the use of the whole-cell voltage-clamp technique. 2. L-Glutamate at a concentration of 50 microM produced inward non-desensitizing currents at negative holding potentials in nearly every cell tested (83%, n = 18) In physiological solutions, L-glutamate responses reversed at approximately -9 mV, and higher concentrations of this agonist introduced a desensitizing component to the response. 3. At negative holding potentials, kainate (25-125 microM) produced inward currents in all of the cells tested (n = 37). These currents never desensitized, even at high agonist concentrations, and reversed near -6 mV. Currents induced by 50 microM-kainate were reversibly antagonized by kynurenate (100-300 microM) but not by 100 microM-2-amino-5-phosphonovalerate (APV). 4. Quisqualate generated smaller, non-desensitizing currents in only 50% of the cells tested (n = 38). Quisqualate responses reversed in polarity near -4 mV and were maximal at an agonist dose of 25 microM, with higher concentrations introducing a rapidly desensitizing component without a detectable increase in amplitude. Currents produced by quisqualate at a concentration of 50 microM were not antagonized by either 750 microM-kynurenate or 100 microM-APV. 5. N-Methyl-D-aspartate (NMDA) produced inward currents at negative holding potentials in 68% of the cells tested (n = 31), but only when magnesium was excluded from the extracellular medium. NMDA currents were non-desensitizing at agonist concentrations of up to 200 microM, with higher concentrations introducing a rapidly desensitizing component. NMDA (200 microM) responses were blocked by APV (100 microM) and kynurenate (300 microM) and reversed near -1 mV. 6. Responses generated by kainate (50-125 microM) were antagonized by quisqualate (30-250 microM). This antagonism occurred even in cells having no measurable response to quisqualate alone, suggesting the possibility that quisqualate may be acting both as an agonist, in the 50% of the cells that have the quisqualate-specific receptor, and as an antagonist, at the kainate-specific site on all cells.(ABSTRACT TRUNCATED AT 400 WORDS)
机译:1.使用全细胞电压钳技术检查了兴奋性氨基酸应答对从大鼠视网膜分离的神经节细胞的药理特性。 2.在几乎每个测试的细胞中,浓度为50 microM的L-谷氨酸在负保持电位下产生向内的非脱敏电流(83%,n = 18)。在生理溶液中,L-谷氨酸的响应在大约-9 mV时反转,并且更高浓度的这种激动剂对反应引入了脱敏成分。 3.在负保持电位下,海藻酸盐(25-125 microM)在所有测试的细胞中产生内向电流(n = 37)。这些电流即使在高激动剂浓度下也不会脱敏,并且在-6 mV附近反转。由50 microM-红藻氨酸盐诱导的电流被kureurenate(100-300 microM)可逆拮抗,但不受100 microM-2-氨基-5-膦酸戊二酸酯(APV)拮抗。 4. Quisqualate仅在50%的测试电池中产生较小的非脱敏电流(n = 38)。准四边形的响应在-4 mV附近极性反转,在25 microM的激动剂剂量下最大,较高的浓度引入快速脱敏成分,而幅度未检测到增加。浓度为50 microM的喹喹啉产生的电流不会被750 microM kyureurenate或100 microM-APV拮抗。 5. N-甲基-D-天门冬氨酸(NMDA)在68%的测试细胞(n = 31)中以负保持电位产生内向电流,但仅当镁从细胞外培养基中排除时才产生。在高达200 microM的激动剂浓度下,NMDA电流不会脱敏,更高的浓度会引入快速脱敏成分。 NMDA(200 microM)响应被APV(100 microM)和kureurenate(300 microM)阻断,并在-1 mV附近反转。 6.红藻氨酸(30-250 microM)拮抗海藻酸盐(50-125 microM)产生的反应。这种拮抗作用甚至发生在仅对喹喹啉单药没有可测量的反应的细胞中,这暗示了喹喹药可能在激动剂中既有激动剂,也有50%的具有喹喹特异特异性受体的细胞,同时又是拮抗剂。所有单元格上的特定站点。(摘要以400字截断)

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