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多胺有助于钙刺激脑微粒组分中天冬氨酸的释放。

Polyamines contribute to calcium-stimulated release of aspartate from brain particulate fractions.

作者信息

Bondy S C, Walker C H

出版信息

Brain Res. 1986 Apr 16;371(1):96-100. doi: 10.1016/0006-8993(86)90814-0.

DOI:10.1016/0006-8993(86)90814-0
PMID:2871896
Abstract

The calcium-stimulated release of several neurotransmitters has been studied in crude synaptosomal preparations following accumulation of various radioactively labeled neurotransmitters or their precursors. The high affinity uptake of D-aspartate, gamma-aminobutyric acid (GABA) and dopamine was not modulated in the presence of 5 mM of difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase (ODC). Depolarization-induced calcium influx caused release of labeled compounds. In the case of D-aspartate, this process was inhibited by DFMO. This major inhibition was completely reversed in the presence of 0.5 mM putrescine, the product of ODC-mediated catabolism of ornithine. This effect could not be shown for the depolarization-related release of dopamine, GABA or acetylcholine. In our preparation, a direct effect of the depolarizing medium upon levels of synaptosomal ODC could not be demonstrated, and the 50 mM K+-stimulated entry of 45Ca into the synaptosomal fraction was not inhibited by DFMO. These data suggest that polyamines are involved in the regulation of neurotransmitter release within certain classes of neurons.

摘要

在积累了各种放射性标记的神经递质或其前体之后,已在粗制突触体制剂中研究了几种神经递质的钙刺激释放。在存在5 mM二氟甲基鸟氨酸(DFMO)(鸟氨酸脱羧酶(ODC)的特异性抑制剂)的情况下,D-天冬氨酸、γ-氨基丁酸(GABA)和多巴胺的高亲和力摄取未受到调节。去极化诱导的钙内流导致标记化合物的释放。就D-天冬氨酸而言,该过程受到DFMO的抑制。在存在0.5 mM腐胺(ODC介导的鸟氨酸分解代谢产物)的情况下,这种主要抑制作用完全逆转。对于多巴胺、GABA或乙酰胆碱的去极化相关释放,未显示出这种效应。在我们的制剂中,未证明去极化介质对突触体ODC水平有直接影响,并且50 mM K +刺激的45Ca进入突触体部分不受DFMO抑制。这些数据表明多胺参与了某些类型神经元内神经递质释放的调节。

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