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Objective: The control of saliva secretion is mainly under parasympathetic control. The submandibular ganglion (SMG) is a parasympathetic ganglion which receives inputs from preganglionic cholinergic neurons, and innervates the submandibular salivary gland to control saliva secretion. The aim of this study was to investigate if adrenomedullin (ADM) and/or calcitonin gene-related peptide (CGRP) modulate voltage-dependent calcium channel (VDCCs) current (I(Ca)) in SMG., Design: The profile of CGRP and ADM actions in SMG was studied using the whole-cell configuration of the patch-clamp technique., Results: Both ADM and CGRP facilitated I(Ca). These facilitations were attenuated by intracellular dialysis of the anti-Gα(s)-protein and pretreatment of SQ22536 (an adenylate cyclase inhibitor)., Conclusions: ADM and CGRP facilitates VDCCs mediated by Gα(s)-protein and adenylate cyclase in SMG., (Copyright © 2010. Published by Elsevier Ltd.)

Objective: Neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), promote neuronal development and neuronal survival, but their mechanisms remain controversial. This study aimed to investigate the hypothesis that NGF and BDNF interfere with angiotensin-II- and glutamate-induced facilitation of voltage-dependent Ca(2+) channels (VDCCs) in nucleus tractus solitarius (NTS) neurons., Design: The profile of NGF and BDNF actions in acutely dissociated rat NTS was studied using the whole-cell configuration of the patch-clamp technique., Results: Pretreatment with NGF and BDNF attenuated angiotensin-II-induced facilitation of VDCCs, but did not attenuate glutamate-induced facilitation of the L-type VDCC current in NTS neurons. NGF-induced attenuation was antagonised by pretreatment with a tyrosine kinase A (TrkA) receptor antagonist K-252a., Conclusions: NGF attenuated angiotensin-II-induced facilitation of L-type VDCCs mediated by TrkA receptors in NTS neurons.

The control of saliva secretion is mainly under parasympathetic control, although there also could be a sympathetic component. Sympathetic nerves are held to have a limited action in secretion in submandibular glands because, on electrical stimulation, only a very small increase to the normal background, basal secretion occurs. Parasympathetic stimulation, on the other hand, caused a good flow of saliva with moderate secretion of acinar mucin, plus an extensive secretion of granules from the granular tubules. The submandibular ganglion (SMG) is a parasympathetic ganglion which receives inputs from preganglionic cholinergic neurons, and innervates the submandibular salivary gland to control saliva secretion. Neurotransmitters and neuropeptides acting via G-protein coupled receptors (GPCRs) change the electrical excitability of neurons. In these neurons, many neurotransmitters and neuropeptides modulate voltage-dependent calcium channels (VDCCs). The modulation is mediated by a family of GPCRs acting either directly through the membrane delimited G-proteins or through second messengers. However, the mechanism of modulation and the signal transduction pathway linked to an individual GPCRs depend on the animal species. This review reports how neurotransmitters and neuropeptides modulate VDCCs and how these modulatory actions are integrated in SMG systems. The action of neurotransmitters and neuropeptides on VDCCs may provide a mechanism for regulating SMG excitability and also provide a cellular mechanism of a variety of neuronal Ca(2+)-dependent processes.

Angiotensin II (Ang II) is one of the most important vasoconstrictive hormones but is also known to act as a neuromodulator and a neurotransmitter in the central and peripheral nervous system. The submandibular ganglion (SMG) neuron is a parasympathetic ganglion which receives inputs from preganglionic cholinergic neurons, and innervates the submandibular salivary gland to control saliva secretion. In this study, the effects of Ang II on SMG neurons were investigated using the whole-cell patch clamp technique. Membrane currents evoked by a ramp pulse from +50 to -100 mV (-150 mV/500 ms) were compared in both the absence and presence of Ang II. In eight neurons tested, 1 microM Ang II increased inward currents by 42.0+/-8.2%. The reversal potentials of the Ang II-induced current were 0.2+/-0.6 mV. These increase of inward currents by Ang II were antagonized by losartan, a selective antagonist of AT(1) receptors. Intracellular dialysis with 0.1mM guanosin 5'-O-(2-thiodiphosphate) (GDP-beta-S), a G-proteins blocker, and anti-G(q/11) antibody attenuated Ang II-induced ionic current. In addition, pretreatment of neurons with 10 microM staurosporine (stauro), a protein kinase C (PKC) inhibitor, 0.5 microM PMA, a PKC activator, and 10 microM KN-93, a Ca2+/calmodulin-dependent protein kinase II (CaM K II) inhibitor, attenuated Ang II-induced ionic current in SMG neurons. The data presented here demonstrated that Ang II-induced ionic current via G(q/11)-proteins involving both PKC and CaM K II pathways in SMG neurons.