μ-opioid presynaptic inhibition of GABA release in rat ventrolateral orbital cortex neurons
会议名称：《中国神经科学学会第四次会员代表大会暨第七届全国学术会议》
会议日期：2007年
学科分类：0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
基 金：supported by the National Natural Science Foundation of China(No.30570592) Natural Science Foundation of Shanxi province(No.2005C235)
关 键 词：ventrolateral orbital cortex mIPSCs DAMGO CTOP whole-cell patch clamp
摘 要：正Previous studies have indicated that the ventrolateral orbital cortex（VLO） is involved in modulation of nociception as part of an endogenous analgesic system consisting of the spinal cord-nucleus submedius（Sm）-VLO-periaqueductal gray（PAG）-spinal cord *** of morphine into the VLO depresses the rat tail-flick reflex and suggests that the GABAergic modulation may be involved in the VLO morphine-induced *** provide electrophysiological evidence for the GABAergic modulation mechanism,the present study examined whether the presynapticμ-opioid activation inhibited release of the GAB A neurotransmitter in rat VLO *** TTX,a voltage-dependent Na+ channel blocker and kynurentic acid,a non-selective excitatory amino acid receptor antagonist,pharmacologically separated spontaneous GABAergic miniature inhibitory postsynaptic currents（mIPSCs） were recorded using the whole-cell patch clamp *** results showed that DAMGO,a specificμ-opioid receptor agonist,inhibited mlPSCs frequency in a dose-dependent manner without affecting mIPSC amplitude in the same VLO *** presynaptic opioid effect was blocked by CTOP,a specificμ-opioid receptor *** alone application did not affect the mIPSC amplitude or *** results provide support for the hypotheses that GABAergic modulation is involved in the opioidinduced antinociception,i.e.,theμ-opioid receptor activation presynaptically inhibits the inhibitory effect of GABAergic neurons on the projection neurons leading to activation of the VLO-PAG brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.