Shapiro M S, Hille B
Department of Physiology and Biophysics, University of Washington, Seattle 98195.
Neuron. 1993 Jan;10(1):11-20. doi: 10.1016/0896-6273(93)90237-l.
We studied inhibition of N-type Ca2+ channels in rat superior cervical ganglion neurons by substance P (SP) and somatostatin-14 (Som). In whole-cell clamp, 70 of 82 acutely dissociated neurons showed inhibition (mean 37%) by 500 nM SP, and 54 of 61 showed inhibition by 240 nM Som (mean 57%). Pertussis toxin (PTX) blocked Som but not SP inhibition; intracellular dialysis with 2 mM GDP-beta-S attenuated inhibition with either peptide. Inhibition was voltage dependent with Som but not with SP. Neurokinin A (1 microM) or B was without effect, implicating NK1 tachykinin receptors. In cell-attached patches with bath-applied drugs, to test for a diffusible messenger, inhibition by SP or Som was only 8%. Thus, SP signaling is voltage independent and PTX insensitive; Som inhibition is voltage dependent and PTX sensitive; and both are membrane delimited.
我们研究了P物质（SP）和生长抑素-14（Som）对大鼠颈上神经节神经元中N型钙通道的抑制作用。在全细胞钳制中，82个急性解离神经元中有70个被500 nM的SP抑制（平均37%），61个中有54个被240 nM的Som抑制（平均57%）。百日咳毒素（PTX）阻断了Som的抑制作用，但未阻断SP的抑制作用；用2 mM GDP-β-S进行细胞内透析可减弱两种肽的抑制作用。Som的抑制作用具有电压依赖性，而SP的抑制作用则无电压依赖性。神经激肽A（1 μM）或神经激肽B无作用，提示为NK1速激肽受体。在使用浴槽给药的细胞贴附式膜片中，为了检测可扩散信使，SP或Som的抑制作用仅为8%。因此，SP信号传导不依赖电压且对PTX不敏感；Som的抑制作用依赖电压且对PTX敏感；两者均受膜限制。
