Morphine-induced μ-opioid receptor desensitization
Morphine-induced μ-opioid receptor desensitization
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DOI：
10.1124/mol.105.013185
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发表时间：
2005-10-01
影响因子：
3.6
通讯作者：
Williams, JT
中科院分区：
文献类型：
--
作者：
Dang, VC;Williams, JT
吗啡已被广泛接受为维持信号传导的阿片激动剂，因为它不会引起受体脱敏或内化。这一概念导致了一种假设，即长期吗啡治疗启动了下游适应，这些适应是耐受性和依赖性的基础。本研究使用蓝斑神经元的全细胞记录来测量吗啡诱导的钾电流。结果表明，吗啡确实引起短期脱敏。吗啡诱导的脱敏作用比[MET]（5）-脑啡肽（ME）诱导的脱敏作用慢且小。在短暂应用饱和浓度的ME后，吗啡诱导的电流较小，未观察到脱敏。在吗啡处理的动物的组织中，吗啡诱导的峰值电流与未处理的动物相同，但促进了吗啡诱导的脱敏。结果表明，吗啡，像其他激动剂，可以启动受体脱敏，以减少信号。
Morphine has been widely accepted as the opioid agonist that sustains signaling because it does not cause receptor desensitization or internalization. This notion has led to the hypothesis that long-term morphine treatment initiates downstream adaptations that underlie tolerance and dependence. This study uses whole-cell recordings from neurons in the locus ceruleus to measure the potassium current induced by morphine. The results show that morphine does cause short-term desensitization. The desensitization induced by morphine was slower and smaller then that induced by [MET](5)-enkephalin ( ME). After a brief application of a saturating concentration of ME, the current induced by morphine was smaller, and desensitization was not observed. In tissue taken from morphine-treated animals, the peak current induced by morphine was the same as in untreated animals, but morphine-induced desensitization was facilitated. The results suggest that morphine, like other agonists, can initiate receptor desensitization to decrease signaling.