Kim C J, Rhee J S, Akaike N
Department of Physiology, Kyung Hee University College of Medicine, Seoul, Korea.
J Neurophysiol. 1997 Mar;77(3):1418-24. doi: 10.1152/jn.1997.77.3.1418.
The effect of mu-type opioid receptor agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 188 PAG neurons tested, the HVA Ca2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of omega-conotoxin-GVIA occluded the inhibitory effect of DAMGO approximately 70%. So, HVA Ca2+ channels inhibited by DAMGO were mainly the N-type Ca2+ channels. The inhibitory effect of DAMGO on HVA Ca2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8-10 h, suggesting that DAMGO modulation on N-type Ca2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that mu-type opioid receptor modulates N-type HVA Ca2+ channels via PTX-sensitive G proteins in PAG neurons of rats.
采用制霉菌素穿孔膜片钳记录模式，在电压钳条件下研究了μ型阿片受体激动剂D-Ala2，N-MePhe4，Gly5-ol-脑啡肽（DAMGO）对离体大鼠中脑导水管周围灰质（PAG）神经元高电压激活（HVA）Ca2+通道的影响。在188个被检测的PAG神经元中，38个神经元（32%）的HVA Ca2+通道被DAMGO抑制（DAMGO敏感细胞），另外80个神经元（68%）不受DAMGO影响（DAMGO不敏感细胞）。DAMGO不敏感细胞中N型、P型、L型、Q型和R型Ca2+通道成分分别占总Ca2+通道电流的26.9%、37.1%、22.3%、7.9%和5.8%。DAMGO敏感细胞的通道成分分别为45.6%、25.7%、21.7%、4.6%和2.4%。DAMGO敏感神经元的HVA Ca2+电流被DAMGO以浓度、时间和电压依赖性方式抑制。应用ω-芋螺毒素-GVIA可阻断DAMGO约70%的抑制作用。因此，被DAMGO抑制的HVA Ca2+通道主要是N型Ca2+通道。用百日咳毒素（PTX）预处理8-10小时几乎完全阻断了DAMGO对HVA Ca2+通道的抑制作用，表明DAMGO对大鼠PAG神经元N型Ca2+通道的调节是由PTX敏感的G蛋白介导的。这些结果表明，μ型阿片受体通过PTX敏感的G蛋白在大鼠PAG神经元中调节N型HVA Ca2+通道。
