吗啡和纳洛酮对钾离子刺激大鼠纹状体切片释放甲硫氨酸脑啡肽的影响。

Effects of morphine and naloxone on the K+-stimulated release of methionine-enkephalin from slices of rat corpus striatum.

作者信息

Sawynok J, Labella F S, Pinsky C

出版信息

Brain Res. 1980 May 12;189(2):483-93. doi: 10.1016/0006-8993(80)90107-9.

Abstract

Methionine-enkephalin (ME) released from superfused slices of rat corpus striatum was estimated by radioimmunoassay (RIA). The basal release of 2.5 +/- 0.2 pmol/g/min (0.15% of content per min) was increased approximately 3-fold upon exposure of tissue to 30 mM K+ for 5 min. This increase in release was not observed in the absence of Ca2+. Both morphine (10(-5) M) and (-)-naloxone (10(-5) and 10(-6) M) significantly depressed the release of ME evoked by 30 mM K+ did not alter basal release. The (+)-isomer of naloxone, which lacks opiate antagonist activity, did not affect basal or evoked release. A consistent depression of release was not observed when 47 mM K+ was used to evoke the release of ME. The issue of whether a feedback mechanism controls the release of ME from the striatum cannot be resolved until it is known whether the effect of morphine and naloxone on ME release are mediated by opiate or non-opiate mechanisms.

摘要

通过放射免疫分析法（RIA）测定了从大鼠纹状体灌流切片中释放的甲硫氨酸脑啡肽（ME）。基础释放量为2.5±0.2皮摩尔/克/分钟（每分钟含量的0.15%），当组织暴露于30 mM K⁺ 5分钟时，释放量增加了约3倍。在没有Ca²⁺ 的情况下未观察到这种释放增加。吗啡（10⁻⁵ M）和（-）-纳洛酮（10⁻⁵ 和10⁻⁶ M）均显著抑制了由30 mM K⁺ 诱发的ME释放，但不改变基础释放。缺乏阿片类拮抗剂活性的纳洛酮（+）-异构体不影响基础释放或诱发释放。当使用47 mM K⁺ 诱发ME释放时，未观察到一致的释放抑制。在了解吗啡和纳洛酮对ME释放的影响是由阿片类还是非阿片类机制介导之前，无法解决反馈机制是否控制纹状体中ME释放的问题。