PRESYNAPTIC ALPHA-2 ADRENOCEPTORS INHIBIT GLUTAMATE RELEASE FROM RAT SPINAL-CORD SYNAPTOSOMES
PRESYNAPTIC ALPHA-2 ADRENOCEPTORS INHIBIT GLUTAMATE RELEASE FROM RAT SPINAL-CORD SYNAPTOSOMES
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DOI：
10.1111/j.1471-4159.1993.tb03180.x
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发表时间：
1993-02-01
影响因子：
4.7
通讯作者：
ITOH, T
中科院分区：
文献类型：
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作者：
KAMISAKI, Y;HAMADA, T;ITOH, T
使用从大鼠脊髓制备的突触体研究了神经末梢氨基酸释放的突触前调节。内源性谷氨酸 (Glu)、天冬氨酸 (Asp) 和 γ-氨基丁酸 (GABA) 的基础释放量分别为 34.6、21.5 和 10.0 pmol/min/mg 蛋白质。暴露于去极化浓度的 KCl (30 mM) 会引起 Glu、Asp 和 GABA 释放分别增加 2.7、1.5 和 2.9 倍。可乐定将 K+ 诱发的 Glu 溢出降低至对照溢出的 5±6%，效力 (IC50) 为 17 nM，但它不影响 K+ 诱发的 Asp、GABA 溢出及其基础释放。类似地，去甲肾上腺素抑制 K+ 引起的 Glu 溢出，尽管是去氧肾上腺素。异丙肾上腺素没有效果。可乐定的抑制作用被α2-肾上腺素受体拮抗剂、萝芙素、育亨宾和咪唑克生抵消，无论咪唑啉的结构如何。由于 Glu 被认为是初级传入神经递质，可在脊髓中传递伤害性和非伤害性刺激，因此这些数据表明部分 Glu 释放可能通过位于初级传入末梢的 α2 肾上腺素能系统受去甲肾上腺素能系统调节。
The presynaptic regulation of amino acid release from nerve terminals was investigated using synaptosomes prepared from the rat spinal cord. The basal releases of endogenous glutamate (Glu), aspartate (Asp), and gamma-aminobutyric acid (GABA) were 34.6, 21.5, and 10.0 pmol/min/mg of protein, respectively. Exposure to a depolarizing concentration of KCl (30 mM) evoked 2.7-, 1.5-, and 2.9-fold increases in Glu, Asp, and GABA release, respectively. Clonidine reduced the K+-evoked overflow of Glu to 5 6% of the control overflow with a potency (IC50) of 17 nM, but it did not affect K+-evoked overflow of Asp, GABA, and their basal releases. Similarly, noradrenaline inhibited the K+-evoked overflow of Glu, although phenylephrine. and isoproterenol showed no effect. The inhibitory effect of clonidine was counteracted by alpha2-adrenoceptor antagonists, rauwolscine, yohimbine, and idazoxan, regardless of the imidazoline structures. Because Glu is considered a neurotransmitter of primary afferents that transmit both nociceptive and nonnociceptive stimuli in the spinal cord, these data suggest that part of Glu release may be regulated by the noradrenergic system through alpha2 adrenoceptors localized on the primary afferent terminals.