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Opioid inhibition of rat periaqueductal grey neurones with identified projections to rostral ventromedial medulla in vitro.

机译:阿片类药物对大鼠导水管周围灰色神经元的抑制作用,并在体外已确定对延髓前延髓质延髓的投射。

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摘要

1. Rat caudal periaqueductal grey (PAG) output neurones containing rhodamine microspheres, retrogradely transported from an injection site in the rostral ventromedial medulla (RVM), were visualized in brain slices and recorded from using whole-cell patch clamp techniques. 2. The specific GABAB receptor agonist baclofen (10 microM) produced an outward current or hyperpolarization in fifty out of fifty-six caudal PAG output neurones. In 44% of these baclofen-sensitive neurones, the opioid agonist methionine enkephalin (30 microM) also produced an outward current or hyperpolarization. The opioid current reversed polarity at -104 mV and could also be produced by DAMGO, an agonist selective for the mu-subtype of opioid receptor. 3. Opioid-responding output neurones were not distributed uniformly in the caudal PAG. In horizontal slices containing lateral PAG, 56% of output neurones were inhibited by opioids, as compared with only 14% of the output neurones in slices containing ventrolateral PAG. 4. These observations are consistent with opioid disinhibition of ventrolateral PAG neurones projecting to the RVM as the predominant mechanism underlying opioid-induced analgesia in the PAG. The role of opioid receptors found on a major proportion of the output neurones in the lateral PAG remains to be established, but is assumed not be related to modulation of nociceptive function.
机译:1.在脑切片中可视化包含从罗氏腹膜延髓(RVM)注射部位逆行转运的罗丹明微球的大鼠尾部导水管周围灰色(PAG)输出神经元,并通过使用全细胞膜片钳技术进行记录。 2.特定的GABA B受体激动剂巴氯芬(10 microM)在56个尾部PAG输出神经元中的50个产生了外向电流或超极化。在这些对巴氯芬敏感的神经元中,有44%的阿片类激动剂蛋氨酸脑啡肽(30 microM)也产生外向电流或超极化现象。阿片类药物电流在-104 mV时极性相反,也可由DAMGO产生,DAMGO是对阿片类药物受体的mu亚型有选择性的激动剂。 3.阿片样物质输出神经元在尾部PAG中分布不均匀。在含有外侧PAG的水平切片中,阿片类药物抑制了56%的输出神经元,而在含有腹侧PAG的切片中仅抑制了14%的输出神经元。 4.这些观察结果与向RVM投射的腹侧PAG神经元的阿片类药物抑制作用相一致,这是阿片类药物引起的PAG镇痛作用的主要机制。在外侧PAG的大部分输出神经元中发现的阿片受体的作用尚待确定,但假定与伤害感受功能的调节无关。

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