Abstract
It is established that neuropeptide Y (NPY) is a transmitter of parasympathetic secretory impulses in submandibular gland. The neuropeptides substance P, vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) are likely mediators of secretory parasympathetic responses of the gland. Previously, we have shown that substance P, VIP and CGRP modulate voltage-dependent Ca2+ channels (VDCCs) in hamster submandibular ganglion (SMG) neurons. In this study, we attempt to characterize the effect of NPY on VDCCs current using Ba2+ (IBa) in SMG neurons. Application of NPY caused both facilitation and inhibition of L-type and N/P/Q-type IBa, respectively. Intracellular dialysis of the Gαs-protein antibody attenuated the NPY-induced facilitation of IBa. The adenylate cyclase (AC) inhibitor, as well as protein kinase A (PKA) inhibitor attenuated the NPY-induced facilitation of IBa. Intracellular dialysis of the Gαi-protein antibody attenuated the NPY-induced inhibition of IBa. Application of a strong depolarizing voltage prepulse attenuated the NPY-induced inhibition of IBa. These results indicate that NPY facilitates L-type VDCCs via Gαs-protein involving AC and PKA. On the other hand, NPY also inhibits N/P/Q-type VDCCs via Gαi-protein βγ subunits in the SMG neurons.
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