Opioid receptor activation attenuates nicotinic enhancement of spontaneous GABA release in lateral spiriform nucleus of the chick.
Opioid receptor activation attenuates nicotinic enhancement of spontaneous GABA release in lateral spiriform nucleus of the chick.
复制标题
阿片受体激活减弱了雏鸡侧螺状核中自发 GABA 释放的烟碱增强作用。
DOI：
10.1016/s0006-8993(02)03837-4
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发表时间：
2003
期刊：
影响因子：
2.9
通讯作者：
Chiappinelli,VincentA
中科院分区：
文献类型：
--
作者：
Nong,Yi;Sorenson,EvaM;Chiappinelli,VincentA
我们研究了阿片类药物对尼古丁增强小鸡外侧螺旋形核（SpL）突触前末梢自发释放GABA的影响。使用脑切片中SpL神经元的全细胞记录来监测自发GABA释放。尼古丁（1 μM）使GABA事件的频率增加8倍，而不改变其振幅，这与突触前末梢释放GABA的增加一致。l-脑啡肽（1 μM）阻断尼古丁对突触前GABA释放的这些作用，阿片拮抗剂纳洛酮（100 nM）拮抗l-脑啡肽的作用。选择性mu激动剂DAMGO（300 nM）也减弱尼古丁介导的GABA释放增强，mu选择性拮抗剂CTOP（1 μM）阻断DAMGO的作用。相比之下，κ阿片激动剂U 50488（3 μM）和δ阿片激动剂DPDPE（1 μM）没有影响。结果表明，突触前释放GABA的SpL可以调节烟碱激动剂和μ阿片类药物。虽然μ阿片类药物本身对GABA释放的影响很小，但它们能够阻断尼古丁通常产生的GABA释放的显着增强。由于胆碱能神经和脑啡肽能神经都存在于SpL中，这两种神经递质系统的相互作用可能有助于精确地调节GABA在该脑区的释放。
We examined the effects of opioids on the nicotinic enhancement of spontaneous GABA release from presynaptic terminals in the lateral spiriform nucleus (SpL) of the chick. Whole cell recordings from SpL neurons in brain slices were used to monitor spontaneous GABA release. Nicotine (1 μM) produced an 8-fold increase in the frequency of GABA events without changing their amplitude, consistent with an increase of GABA release from presynaptic terminals. l-enkephalin (1 μM) blocked these effects of nicotine on presynaptic GABA release, and the opioid antagonist naloxone (100 nM) antagonized the actions of l-enkephalin. The selective mu agonist DAMGO (300 nM) also attenuated the nicotine-mediated enhancement of GABA release, and the mu selective antagonist CTOP (1 μM) blocked the actions of DAMGO. In contrast, the kappa opioid agonist U50488 (3 μM) and the delta opioid agonist DPDPE (1 μM) had no effect. The results demonstrate that presynaptic release of GABA in the SpL can be regulated by both nicotinic agonists and mu opioids. While mu opioids have little effect on GABA release by themselves, they are able to block the marked enhancement of GABA release normally produced by nicotine. Since both cholinergic and enkephalinergic nerves are present in the SpL, the interactions of these two neurotransmitter systems may serve to precisely regulate GABA release in this brain region.