Regional release of [3H]dopamine from rat brain in vitro: effects of opioids on release induced by potassium, nicotine, and L-glutamic acid.
Regional release of [3H]dopamine from rat brain in vitro: effects of opioids on release induced by potassium, nicotine, and L-glutamic acid.
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大鼠脑体外 [3H] 多巴胺的区域释放：阿片类药物对钾、尼古丁和 L-谷氨酸诱导的释放的影响。
DOI：
10.1139/y83-005
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发表时间：
1983
影响因子：
2.1
通讯作者：
K. Jhamandas
中科院分区：
文献类型：
--
作者：
M. Marien;J. Brien;K. Jhamandas
以往的研究表明，大鼠脑内多巴胺（DA）的释放可能对阿片类药物的调节敏感，包括内源性阿片肽（脑啡肽和内啡肽）。本研究探讨了吗啡和脑啡肽类似物D-Ala 2-Met 5-enkephalinamide（DALA）对大鼠脑区灌流切片释放放射性标记DA的影响。预载的[3 H]DA的释放被诱发从尾壳核（CP）切片的应用钾（K+），尼古丁（NIC），或L-谷氨酸（L-GLU）。用L-GLU诱发嗅核（NA）、嗅结节（OT）和黑质（SN）脑片[~ 3 H]DA的释放。K+和NIC均引起CP脑片[~ 3 H]DA的浓度相关性释放。K+诱导的释放仅部分依赖于钙离子（Ca 2+），而NIC诱导的释放完全不依赖于Ca 2+。吗啡和DALA均不影响K+或NIC诱发的[3 H]DA释放。L-GLU使CP、NA、OT和SN切片释放[~ 3 H]DA，并呈浓度依赖性。在所有四个脑区中，这种释放是（a）Ca 2+依赖性的，（B）被低浓度的镁（Mg 2+）强烈抑制，（c）大于由D-GLU诱发的释放，（d）被假定的L-GLU受体拮抗剂谷氨酸二乙酯（GDEE）减弱，（e）对河豚毒素（TTX）不敏感（SN除外）。吗啡产生了显着抑制L-谷氨酸诱发的[3 H]DA释放从所有四个区域。纳洛酮本身对L-GLU诱发的[3 H]DA释放无显著影响，但可阻断吗啡对CP释放的抑制作用，但在其他区域则无此作用。左啡烷和右啡烷在减少CP切片中谷氨酸刺激的[3 H]DA释放方面是等效的。DALA没有影响L-GLU诱导的释放在任何大脑区域检查。结果表明，L-GLU通过作用于Mg 2+敏感的谷氨酸受体引起DA的区域释放。这种释放通过对纳洛酮不敏感的机制被吗啡选择性地修饰。
Previous studies have suggested that the release of dopamine (DA) in the rat brain may be sensitive to modulation by opioid agents, including the endogenous opioid peptides (enkephalins and endorphins). The present study examined the effects of morphine and the enkephalin analogue D-Ala2-Met5-enkephalinamide (DALA) on the release of radiolabeled DA from superfused slices of rat brain regions. The release of preloaded [3H]DA was evoked from slices of the caudate-putamen (CP) by application of potassium (K+), nicotine (NIC), or L-glutamic acid (L-GLU). The release of [3H]DA from slices of the nucleus accumbens (NA), olfactory tubercle (OT), and substantia nigra (SN) was evoked by L-GLU. Both K+ and NIC evoked a concentration-related release of [3H]DA from CP slices. K+-induced release was only partially dependent on calcium (Ca2+), while NIC-evoked release was completely Ca2+ independent. Neither morphine nor DALA influenced the release of [3H]DA evoked by K+ or NIC. L-GLU produced a concentration-dependent release of [3H]DA from slices of CP, NA, OT, and SN. In all four brain regions, this release was (a) Ca2+-dependent, (b) strongly inhibited by low concentrations of magnesium (Mg2+), (c) greater than the release evoked by D-GLU, (d) attenuated by the putative L-GLU receptor antagonist glutamic acid diethylester (GDEE), and (e) insensitive to tetrodotoxin (TTX) except in the SN. Morphine produced a significant inhibition of L-GLU-evoked [3H]DA release from all four regions. Naloxone, which by itself had no significant effect on the L-GLU-evoked release of [3H]DA, blocked the inhibitory effect of morphine on this release in the CP but not in the other regions. Levorphanol and dextrorphan were equipotent in reducing the glutamate-stimulated release of [3H]DA from CP slices. DALA had no effect on L-GLU-induced release in any of the brain regions examined. The results indicate that L-GLU provokes regional release of DA by acting at a Mg2+-sensitive glutamate receptor. This release is selectively modified by morphine through a mechanism which is insensitive to naloxone.