Song S Y, Iwashita S, Noguchi K, Konishi S
Laboratory of Cellular Physiology, Mitsubishi Kasei Institute of Life Sciences, Tokyo, Japan.
Neurosci Lett. 1988 Dec 19;95(1-3):143-8. doi: 10.1016/0304-3940(88)90647-7.
The action of substance P (SP) on a rat pancreatic acinar cell line, AR4-2J, was examined using the whole-cell voltage-clamp technique. Pressure application of SP evoked inward currents accompanying increased membrane conductance. The SP-induced response was suppressed in Ca2+-free or low-Na+ solution. Treatment of cells with caffeine or A23187 produced a transient inward current and depressed the response to SP. Intracellular application of inositol 1,4,5-trisphosphate or guanosine 5'-O-(3-thiotriphosphate) elicited sustained inward currents and suppressed the SP-induced response. The results suggest that activation of SP receptors stimulates the formation of inositol phosphates via a guanine nucleotide-binding protein and leads to the rise in intracellular Ca2+, thereby activating a cation conductance in AR4-2J cells.
采用全细胞膜片钳技术研究了P物质（SP）对大鼠胰腺腺泡细胞系AR4-2J的作用。施加SP可诱发内向电流并伴有膜电导增加。在无钙或低钠溶液中，SP诱导的反应受到抑制。用咖啡因或A23187处理细胞可产生瞬时内向电流并抑制对SP的反应。细胞内应用肌醇1,4,5-三磷酸或鸟苷5'-O-(3-硫代三磷酸)可引发持续的内向电流并抑制SP诱导的反应。结果表明，SP受体的激活通过鸟嘌呤核苷酸结合蛋白刺激肌醇磷酸的形成，导致细胞内Ca2+升高，从而激活AR4-2J细胞中的阳离子电导。
