Nakajima Y, Nakajima S, Inoue M
Department of Biological Sciences, Purdue University, West Lafayette, IN 47907.
Proc Natl Acad Sci U S A. 1988 May;85(10):3643-7. doi: 10.1073/pnas.85.10.3643.
Substance P excites neurons by suppressing inward rectification channels. We have investigated whether the substance P receptor interacts with the inward rectification channels through a guanine nucleotide-binding protein (G protein) by using dissociated cultured neurons from the nucleus basalis of newborn rats. During intracellular application of guanosine 5'-[gamma-thio]triphosphate and 5'-guanylyl imidodiphosphate, hydrolysis-resistant GTP analogues that irreversibly stimulate G proteins, substance P application almost irreversibly suppressed the inward rectification channels. Pretreatment with pertussis toxin did not significantly influence substance P action. Intracellular application of cAMP and 3-isobutyl-1-methylxanthine or of 9-(tetrahydro-2-furyl)adenine (SQ 22,536), an inhibitor of adenylate cyclase, did not alter the substance P-induced response. We conclude that the inhibition of inward rectification channels by substance P is mediated through a G protein. However, the effect is not mediated through adenylate cyclase or the cAMP system. This G protein, which is insensitive to pertussis toxin, could be an unidentified G protein.
P物质通过抑制内向整流通道来兴奋神经元。我们利用新生大鼠基底核的解离培养神经元,研究了P物质受体是否通过鸟嘌呤核苷酸结合蛋白(G蛋白)与内向整流通道相互作用。在细胞内应用鸟苷5'-[γ-硫代]三磷酸和5'-鸟苷酰亚胺二磷酸(两种不可逆刺激G蛋白的抗水解GTP类似物)期间,应用P物质几乎不可逆地抑制了内向整流通道。用百日咳毒素预处理对P物质的作用没有显著影响。细胞内应用cAMP和3-异丁基-1-甲基黄嘌呤或应用9-(四氢-2-呋喃基)腺嘌呤(SQ 22,536,一种腺苷酸环化酶抑制剂)并没有改变P物质诱导的反应。我们得出结论,P物质对内向整流通道的抑制作用是通过一种G蛋白介导的。然而,这种作用不是通过腺苷酸环化酶或cAMP系统介导的。这种对百日咳毒素不敏感的G蛋白可能是一种尚未鉴定的G蛋白。