Foucart S, Bleakman D, Bindokas V P, Miller R J
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois.
J Pharmacol Exp Ther. 1993 May;265(2):903-9.
We examined the effects of neuropeptide Y (NPY) and pancreatic polypeptide on calcium currents (ICa) in acutely dissociated neurons from the adult rat superior cervical ganglion. We found that NPY inhibited the ICa with an estimated IC50 value of 140 nM. This inhibitory effect appeared to be restricted to a subset of cells which were smaller in diameter than the general population. The effect of NPY on the ICa was prevented by pretreatment with pertussis toxin, suggesting the involvement of a GTP-binding protein of the Gi or Go subtype. omega-conotoxin GVIA also occluded the effects of NPY, which suggests that these were directed toward N-type Ca++ channels. The effects of NPY were mimicked by the fragment NPY (13-36) but not by peptide YY, indicating that a receptor distinct from a Y1- or a Y2-like NPY receptor was involved. Finally, we also observed that pancreatic polypeptide inhibited the ICa, suggesting that a pancreatic polypeptide receptor is also present on superior cervical ganglion neurons.
我们研究了神经肽Y(NPY)和胰多肽对成年大鼠颈上神经节急性分离神经元钙电流(ICa)的影响。我们发现NPY抑制ICa,估计半数抑制浓度(IC50)值为140 nM。这种抑制作用似乎仅限于直径小于总体细胞群体的一个细胞亚群。用百日咳毒素预处理可阻止NPY对ICa的作用,提示Gi或Go亚型的GTP结合蛋白参与其中。ω-芋螺毒素GVIA也可阻断NPY的作用,这表明这些作用是针对N型Ca++通道的。NPY(13-36)片段可模拟NPY的作用,但肽YY则不能,这表明涉及一种不同于Y1或Y2样NPY受体的受体。最后,我们还观察到胰多肽抑制ICa,提示颈上神经节神经元上也存在胰多肽受体。