Muscarinic acetylcholine receptor modulation of mu (mu) opioid receptors in adult rat sphenopalatine ganglion neurons.
Muscarinic acetylcholine receptor modulation of mu (mu) opioid receptors in adult rat sphenopalatine ganglion neurons.
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成年大鼠蝶腭神经节神经元中 mu (mu) 阿片受体的毒蕈碱乙酰胆碱受体调节。
DOI：
10.1152/jn.00295.2009
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发表时间：
2010
影响因子：
2.5
通讯作者：
Ruiz-Velasco,Victor
中科院分区：
文献类型：
--
作者：
Margas,Wojciech;Mahmoud,Saifeldin;Ruiz-Velasco,Victor
蝶腭神经节(SPG)神经元代表自主神经系统的副交感神经分支，参与控制脑血流。在本研究中，我们在急性分离的成年大鼠孤束核神经元上研究了Mu(μ)阿片受体(MOR)和M受体(MAChR)与钙通道的偶联机制。采用膜片钳技术的全细胞变种技术，在∼中记录到40-45%的SPG神经元成功地激活了MOR。免疫荧光分析表明，所有SPG神经元均不表达MOR，而M2mAChR在所有神经元中均有明显表达。吗啡和[d-Ala2-N-Me-Phe4-Glycol5]-脑啡肽(DAMGO)的IC50值分别为15.2和56.1 nM，最大钙电流抑制率分别为26.0和38.7%。吗啡或甲氧三乙胺(Oxo-M)分别激活MOR或M2mAChR，可通过偶联G-αI/o蛋白亚基抑制电压依赖性钙电流。吗啡或Oxo-M对神经元的急性长时间暴露(10min)分别导致MOR和M2mAChR的相应脱敏。OXO-M长时间刺激M2mAChR可使吗啡介导的钙电流抑制异源脱敏，且对M2mAChR阻断剂甲氧曲明敏感。而在吗啡或DAMGO作用10min时，未观察到M2mAChR异源脱敏现象。这些结果表明，在大鼠SPG神经元中，M2mAChR的激活可能调节脑血管中阿片类药物的传递，以充分维持脑血流。
The sphenopalatine ganglion (SPG) neurons represent the parasympathetic branch of the autonomic nervous system involved in controlling cerebral blood flow. In the present study, we examined the coupling mechanism between mu (μ) opioid receptors (MOR) and muscarinic acetylcholine receptors (mAChR) with Ca2+channels in acutely dissociated adult rat SPG neurons. Successful MOR activation was recorded in ∼40–45% of SPG neurons employing the whole cell variant of the patch-clamp technique. In addition, immunofluorescence assays indicated that MOR are not expressed in all SPG neurons while M2mAChR staining was evident in all neurons. The concentration-response relationships generated with morphine and [d-Ala2-N-Me-Phe4-Glycol5]-enkephalin (DAMGO) showed IC50values of 15.2 and 56.1 nM and maximal Ca2+current inhibition of 26.0 and 38.7%, respectively. Activation of MOR or M2mAChR with morphine or oxotremorine-methiodide (Oxo-M), respectively, resulted in voltage-dependent inhibition of Ca2+currents via coupling with Gαi/oprotein subunits. The acute prolonged exposure (10 min) of neurons to morphine or Oxo-M led to the homologous desensitization of MOR and M2mAChR, respectively. The prolonged stimulation of M2mAChR with Oxo-M resulted in heterologous desensitization of morphine-mediated Ca2+current inhibition, and was sensitive to the M2mAChR blocker methoctramine. On the other hand, when the neurons were exposed to morphine or DAMGO for 10 min, heterologous desensitization of M2mAChR was not observed. These results suggest that in rat SPG neurons activation of M2mAChR likely modulates opioid transmission in the brain vasculature to adequately maintain cerebral blood flow.
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