Epinephrine and norepinephrine modulate neuronal responses to excitatory amino acids and agonists in frog spinal cord.

Epinephrine and norepinephrine modulate neuronal responses to excitatory amino acids and agonists in frog spinal cord.
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肾上腺素和去甲肾上腺素调节青蛙脊髓中神经元对兴奋性氨基酸和激动剂的反应。

DOI:
10.1002/syn.890010208
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发表时间:
1987
期刊:
Synapse (New York, N.Y.)
影响因子:
--
通讯作者:
Davidoff,RA
Davidoff,RA
中科院分区:
--
文献类型:
--
作者:
Wohlberg,CJ;Hackman,JC;Davidoff,RA

文献摘要

相似文献

通过腹根的蔗糖间隙记录研究了儿茶酚胺肾上腺素 (E) 和去甲肾上腺素 (NE) (1.0–100 μM) 与兴奋性氨基酸对离体灌流青蛙脊髓运动神经元的相互作用。在应用 L-天冬氨酸或 L-谷氨酸之前将脐带暴露于 E 或 NE 30 秒,可减少氨基酸产生的运动神经元去极化。对混合受体激动剂 L-谷氨酸和 L-天冬氨酸的反应减少可能是儿茶酚胺对氨基酸激活特定兴奋性受体的相反作用的结果。因此,E 和 NE 促进了 N-甲基-D-天冬氨酸 (NMDA) 引起的去极化,并抑制了使君子酸产生的去极化。对 NMDA 反应的影响似乎是由 β 肾上腺素受体介导的,因为它被 β 激动剂异丙肾上腺素模拟并被普萘洛尔阻断。对君子草酸去极化的影响似乎需要激活α2-肾上腺素受体;它被 α2 激动剂可乐定和 α-甲基去甲肾上腺素模仿,并被育亨宾和哌罗生拮抗。这些结果对于理解儿茶酚胺对使用兴奋性氨基酸作为递质的脊髓通路反射传递的作用非常重要。
The interaction of catecholamines epinephrine (E) and norepinephrine (NE) (1.0–100 μM) and excitatory amino acids on motoneurons of the isolated superfused frog spinal cord was investigated by sucrose gap recordings from ventral roots. Exposure of the cord to E or NE 30 sec prior to application of L‐aspartate or L‐glutamate reduced the motoneuron depolarizations produced by the amino acids. The reduction of responses to the mixed receptor agonists L‐glutamate and L‐aspartate may be the result of opposite actions of the catecholamines on the activation of specific excitatory receptors by the amino acids. Thus, E and NE facilitated depolarizations caused by application of N‐methyl‐D‐aspartate (NMDA) and depressed those produced by quisqualate. The effect on NMDA responses appeared to ne β‐adrenoceptor mediated because it was mimicked by the β‐agonist isoprotereno and blocked by propranolol. The effect on quisqualate depolarizations appeared to require activation of α2‐adrenoceptors; it was mimicked by the α2‐agonists clonidine and α‐methylnorepinephrine and antagonized by yohimbine and piperoxan. These results are important in understanding the actions of catecholamines on reflex transmission in spinal pathways which use excitatory amino acids as transmitters.