Submandibular Ganglion Neurons Research Articles

Parasympathetic neurons in the human submandibular ganglion

The submandibular ganglion (SMG) contains parasympathetic neurons which innervate the submandibular gland. In this study, immunohistochemistry for vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), choline acetyltransferase (ChAT), dopamine β-hydroxylase (DBH), tyrosine hydroxylase (TH), and the transient receptor potential cation channel subfamily V members 1 (TRPV1) and 2 (TRPV2) was performed on the human SMG. In the SMG, 17.5 % and 8.9 % of parasympathetic neurons were immunoreactive for VIP and TRPV2, respectively. SMG neurons mostly contained ChAT- and DBH-immunoreactivity. In addition, subpopulations of SMG neurons were surrounded by VIP (69.6 %)-, TRPV2 (54.4 %)- and DBH (9.5 %)-immunoreactive (-ir) nerve fibers. SMG neurons with pericellular VIP- and TRPV2-ir nerve fibers were significantly larger than VIP- and TRPV2-ir SMG neurons, respectively. Other neurochemical substances were rare in the SMG. In the human submandibular gland, TRPV1- and TRPV2-ir nerve fiber profiles were seen around blood vessels. Double fluorescence method also demonstrated that TRPV2-ir nerve fiber profiles were located around myoepithelial and acinar cells in the submandibular gland. VIP and TRPV2 are probably expressed by both pre- and post-ganglionic neurons innervating the submandibular and sublingual glands. VIP, DBH and TRPV2 may have functions about regulation of salivary components in the salivary glands and neuronal activity in the SMG.

Imaging the Transport Dynamics of Single Alphaherpesvirus Particles in Intact Peripheral Nervous System Explants from Infected Mice

ABSTRACTAlphaherpesvirus particles travel long distances in the axons of neurons using host microtubule molecular motors. The transport dynamics of individual virions in neurons have been assessed in cultured neurons, but imaging studies of single particles in tissue from infected mice have not been reported. We developed a protocol to image explanted, infected peripheral nervous system (PNS) ganglia and associated innervated tissue from mice infected with pseudorabies virus (PRV). This ex vivo preparation allowed us to visualize and track individual virions over time as they moved from the salivary gland into submandibular ganglion neurons of the PNS. We imaged and tracked hundreds of virions from multiple mice at different time points. We quantitated the transport velocity, particle stalling, duty cycle, and directionality at various times after infection. Using a PRV recombinant that expressed monomeric red fluorescent protein (mRFP)-VP26 (red capsid) and green fluorescent protein (GFP)-Us9 (green membrane protein), we corroborated that anterograde transport in axons occurs after capsids are enveloped. We addressed the question of whether replication occurs initially in the salivary gland at the site of inoculation or subsequently in the neurons of peripheral innervating ganglia. Our data indicate that significant amplification of infection occurs in the peripheral ganglia after transport from the site of infection and that these newly made particles are transported back to the salivary gland. It is likely that this reseeding of the infected gland contributes to massive invasion of the innervating PNS ganglia. We suggest that this “round-trip” infection process contributes to the characteristic peripheral neuropathy of PRV infection.

Neuropeptide Y modulates calcium channels in hamster submandibular ganglion neurons

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.

Differential expression of P2X receptors on neurons from different parasympathetic ganglia

Whole-cell patch clamp recording and immunohistochemistry were used to investigate the expression of P2X receptors on rat parasympathetic ganglion neurons of the otic, sphenopalatine, submandibular, intracardiac and paratracheal ganglia. Neurons from all five ganglia responded to ATP with a rapidly activating, sustained inward current. Neurons of intracardiac and paratracheal ganglia were insensitive to αβ-meATP, while all neurons in the otic and some neurons of sphenopalatine and submandibular ganglia responded. Lowering pH potentiated ATP responses in neurons from all five ganglia. Co-application of Zn 2+ potentiated ATP responses in intracardiac, paratracheal and submandibular ganglion neurons. Immunohistochemistry revealed strong and specific staining for the P2X 2 subunit in all five ganglia and strong P2X 3 staining in otic, sphenopalatine and submandibular ganglia. In conclusion, there is heterogeneity in P2X receptor expression in different parasympathetic ganglia of the rat, but the predominant receptor subtypes involved appear to be homomeric P2X 2 and heteromeric P2X 2/3.

Modulation of voltage-dependent calcium channels by neurotransmitters and neuropeptides in parasympathetic submandibular ganglion 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.

Multiple signal pathways coupling VIP and PACAP receptors to calcium channels in hamster submandibular ganglion neurons

The Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are two novel neuropeptides which produce particular biological effects caused by interaction with G-protein-coupled receptors. We have shown in a previous study where VIP and PACAP 38 inhibit voltage-dependent calcium channel (VDCC) currents (I Ca) via G-proteins in hamster submandibular ganglion (SMG) neurons. In this study, we attempt to further characterize the signal transduction pathways of VIP-and PACAP 38-induced modulation of I Ca. Application of 1 μM VIP and PACAP 38 inhibited I Ca by 33.0±3.1% and 36.8±2.6%, respectively (mean±S.E.M., n=8). Application of strong voltage prepulse attenuated PACAP 38-induced inhibition of I Ca. Pretreatment of cAMP dependent protein kinase (PKA) activator attenuated VIP-induced inhibition, but not the PACAP 38-induced inhibition. Intracellular dialysis of the PKA inhibitor attenuated the VIP-induced inhibition, but not the PACAP 38-induced inhibition. Pretreatment of protein kinase C (PKC) activator and inhibitor attenuated VIP-induced inhibition, but not the PACAP 38-induced inhibition. Pretreatment of cholera toxin (CTX) attenuated PACAP 38-induced inhibition of I Ca. These findings indicate that there are multiple signaling pathways in VIP and PACAP 38-induced inhibitions of I Ca: one pathway would be the VPAC 1/VPAC 2 receptors-induced inhibition involving both the PKA and PKC, and another one concerns the PAC 1 receptor-induced inhibition via G s-protein βγ subunits. The VIP-and PACAP 38-induced facilitation of I Ca can be observed in the SMG neurons in addition to inhibiting of I Ca.

Angiotensin II-induced ionic currents and signalling pathways in submandibular ganglion neurons

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 μM 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 0.1 mM guanosin 5′- O-(2-thiodiphosphate) (GDP-β-S), a G-proteins blocker, and anti-G q/11 antibody attenuated Ang II-induced ionic current. In addition, pretreatment of neurons with 10 μM staurosporine (stauro), a protein kinase C (PKC) inhibitor, 0.5 μM PMA, a PKC activator, and 10 μM KN-93, a Ca 2+/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.

Extracellular ATP-induced calcium channel inhibition mediated by P1/P2Y purinoceptors in hamster submandibular ganglion neurons.

1. The presence and profile of purinoceptors in neurons of the hamster submandibular ganglion (SMG) have been studied using the whole-cell configuration of the patch-clamp technique. 2. Extracellular application of adenosine 5'-triphosphate (ATP) reversibly inhibited voltage-dependent Ca(2+) channel (VDCC) currents (I(Ca)) via G(i/o)-protein in a voltage-dependent manner. 3. Extracellular application of uridine 5'-triphosphate (UTP), 2-methylthioATP (2-MeSATP), alpha,beta-methylene ATP (alpha,beta-MeATP) and adenosine 5'-diphosphate (ADP) also inhibited I(Ca). The rank order of potency was ATP=UTP>ADP>2-MeSATP=alpha,beta-MeATP. 4. The P2 purinoceptor antagonists, suramin and pyridoxal-5-phosphate-6-azophenyl-2', 4'-disulfonic acid (PPADS), partially antagonized the ATP-induced inhibition of I(Ca), while coapplication of suramin and the P1 purinoceptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), virtually abolished I(Ca) inhibition. DPCPX alone partially antagonized I(Ca) inhibition. 5. Suramin antagonized the UTP-induced inhibition of I(Ca), while DPCPX had no effect. 6. Extracellular application of adenosine (ADO) also inhibited I(Ca) in a voltage-dependent manner via G(i/o)-protein activation. 7. Mainly N- and P/Q-type VDCCs were inhibited by both ATP and ADO via G(i/o)-protein betagamma subunits in seemingly convergence pathways.

PACAP-induced depolarizations in hamster submandibular ganglion neurons.

In this study, we have investigated the effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on in vitro hamster submandibular ganglion neurons using the conventional intracellular recording technique. PACAP (10 microM) induced slow depolarizations in approximately 70% of tested cells. PACAP-induced depolarizations were approximately 10 mV in the peak amplitude, and their durations were approximately 10 min. The slow depolarizations were accompanied by a decrease in membrane conductance (gm) at the initial phase and an increase in gm at the peak phase. Membrane input resistance increased by 14.8 +/- 2.2% (mean +/- S.E., max.) of the resting value at the initial phase and decreased by 30.8 +/- 4.3% (max.) at the peak phase. Anodal break spikes were elicited at the initial phase during PACAP-induced depolarization. In one neuron, anodal break spikes were elicited at the peak. Spikes which followed the anodal break spike were also elicited at 4 Hz in the initial phase during the slow depolarizations. The decrease in gm was probably produced by an inhibition of calcium conductance and an inhibition of slow Ca(2+)-activated K+ channels, while the increase in gm might have been produced by an activation of nonselective cation channels. The slow depolarizations by PACAP might be mediated by a membrane-delimited signal transduction cascade involving G protein in the submandibular ganglion neurons.

Angiotensin II-induced inhibition of calcium currents via G(q/11)-protein involving protein kinase C in hamster submandibular ganglion neurons.

Angiotensin II (AngII) 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 systems. In a previous study, we have shown that AngII, mediated by AT(1) receptors, inhibits voltage-dependent calcium channel (VDCC) currents (I(Ca)) via G-proteins in submandibular ganglion (SMG) neurons. In this study, we further characterized the signal transduction of AngII-induced inhibition of I(Ca). Application of 1 microM AngII inhibited I(Ca) by 32.1+/-2.7% (mean+/-S.E.M., n=9). Intracellular dialysis of anti-G(q/11) antibodies attenuated these inhibition (8.8+/-1.3%, n=6). In addition, treatment of protein kinase C (PKC) activator and inhibitor also attenuated these inhibition (8.0+/-0.9 and 9.8+/-0.9%, n=6 and 9, respectively). We therefore conclude that AngII inhibits VDCC via G(q/11)-proteins involving in SMG neurons. In addition, such PKC-dependent pathways mediated mainly L-type VDCC inhibition.

Cyclic AMP-dependent protein kinase-independent angiotensin II-induced inhibition of calcium current in hamster submandibular ganglion neurons.

In a previous study, we demonstrated that angiotensin II (AngII) inhibited voltage-dependent calcium channels (VDCCs) currents (ICa) in hamster submandibular ganglion (SMG) neurons. In sinoatrial node cells, it has been reported that AngII inhibits ICa by suppressing cyclic AMP production. In this study, to investigate the possible involvement of a cyclic AMP-cyclic AMP dependent protein kinase (PKA) pathway in the AngII-induced inhibition of ICa, effects of AngII were examined in SMG neurons after treatment with an activator and inhibitor of PKA. Neither pretreatment of neurons with membrane permeable cyclic AMP nor intracellular dialysis of PKA blocker attenuated the AngII-induced inhibition of ICa. These results indicate that AngII inhibited ICa via a cyclic AMP-PKA-independent mechanism in SMG neurons.

Constitution of calcium channel current in hamster submandibular ganglion neurons.

The submandibular ganglion (SMG) neuron has been well established as the parasympathetic ganglion that innervates the submandibular and sublingual salivary glands. Thus this neuron plays a key role in salivary secretion. In a previous study, we reported that SMG possessed T-, L-, N-, P/Q- and R-type voltage-dependent calcium channels (VDCCs). In this study, we analyzed the contribution of the distinct subtypes of VDCCs currents (ICa) using the whole-cell configuration of the patch clamp technique in SMG neurons. In addition, we also investigated the effects of a strong voltage prepulse on the contributions of the subtypes of VDCCs. In SMG neuronal ICa without a prepulse, the mean percentages of L-, N-, P-, Q- and R-type were 39.7, 31.5, 10.6, 7.1 and 7.9%. In SMG neuronal ICa with prepulse, the mean percentages of L-, N-, P-, Q- and R-type were 37.2, 34.0, 14.0, 7.6 and 7.0%. Thus, these results showed that SMG possess multiple types of VDCCs and that N- and P-type VDCCs are facilitated by a prepulse in SMG neurons.

VIP and PACAP inhibit L-, N- and P/Q-type Ca2+ channels of parasympathetic neurons in a voltage independent manner.

In this study, we investigated the effects of vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide 1-38 (PACAP) on the voltage-gated calcium currents in hamster submandibular ganglion neurons. VIP and PACAP inhibited the high threshold voltage-gated calcium current in a voltage-independent and a concentration-dependent manner via the G protein-mediated pathway. L-, N- and P/Q-type components of the total maximum voltage-gated calcium current accounted for 48.0 +/- 3.1% (n = 4), 35.1 +/- 4.7% (n = 4), and 13.5 +/- 2.3% (n = 3) of the total peak amplitude, respectively. VIP at a concentration of 1 microM inhibited the L-type calcium current by 33.2% +/- 1.4% (n = 4), the N-type current by 31.0 +/- 3.6%, and the P/Q-type current by 3.2 +/- 1.1% (n = 3). PACAP at a concentration of 1 microM inhibited the L-type current by 35.6 +/- 5.7%, the N-type current by 34.4 +/- 3.1% (n = 4), and the P/Q-type current by 6.4 +/- 2.1% (n = 2). However, VIP and PACAP did not inhibit the low threshold voltage-gated (T-type) calcium current. The rank order of potency was PACAP > VIP. In experiments replacing GTP with GDP-beta-S, the inhibitory effects of VIP and PACAP were prevented. In experiments of double-pulse protocol, depolarizing conditioning pulses could not relieve the inhibition of total high threshold voltage-gated calcium currents produced by VIP and PACAP. Therefore, the inhibition of the high threshold voltage-gated calcium channels produced by VIP and PACAP in hamster parasympathetic neurons differed in its mechanisms from that of N-type calcium channels in rat sympathetic neurons.

Angiotensin II-induced inhibition of calcium currents in hamster submandibular ganglion neurons.

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 systems. In a previous study, we have shown that Ang II, via AT1 receptors, induced depolarization by inhibition of M-type K(+) channels and SK channels in submandibular ganglion (SMG) neurons. In this study, we investigated the effects of Ang II on calcium channel current (I(Ca)) in acutely dissociated SMG neurons by the patch-clamp technique using the whole-cell configuration. Ang II inhibited total I(Ca) by 32.1+/-2.7%. The half-maximum inhibitory concentration (IC(50)) of Ang II for inhibiting I(Ca) was 0.8 microM. In the presence of 1 microM losartan, which is a selective antagonist of AT1 receptors, the effect of Ang II was attenuated (7.6+/-1.5%). Application of a strong depolarizing voltage prepulse did not affect the Ang II-induced inhibition of I(Ca) (32.8+/-2.8%). Intracellular dialysis of GDP-beta-S attenuated the inhibition of I(Ca) (6.8+/-2.1%). The mean percentage inhibitions of L-, N- and P/Q-type VDCCs by Ang II were 29.1+/-1.7, 16.3+/-6.0 and 1.2+/-0.8%, respectively, of the total I(Ca).

Kinetic analysis of prepulse facilitation of calcium currents in hamster submandibular ganglion neurons.

The calcium ion influx through voltage-dependent calcium channels (VDCCs) has a vital role in the control of neurotransmitter release and membrane excitability. The modulation of VDCCs controls the extent of calcium entry and thus provides a way of regulating neuronal function. Prepulse facilitation is a phenomenon in which a strong depolarizing pulse induces a form of the VDCCs that exhibits an increased opening probability in response to a given test potential that persists for several seconds after repolarization. In this study, we have studied the characterization of prepulse facilitation of VDCCs currents (Ica) in hamster submandibular ganglion (SMG) neurons, using whole-cell patch clamp recordings. In SMG neurons, application of a strong depolarizing prepulse caused a Ica. In 8 SMG neurons, rate of facilitation was 1.1 +/- 0.1. The greatest value of prepulse facilitation was obtained with prepulse to +100 mV, 10 ms duration in this neuron. The magnitude of facilitation was dependent on changing the interval between the -prepulse and the +prepulse and reached a maximum at a interval of 500 ms.

Decay in prepulse facilitation of calcium channel currents by Gi/o-protein attenuation in hamster submandibular ganglion neurons, but not Gq/11.

The calcium ion influx through voltage-dependent calcium channels (VDCCs) has a vital role in the control of neurotransmitter release and membrane excitability. Prepulse facilitation is a phenomenon in which a strong depolarizing pulse induces a form of the VDCCs that exhibits an increased opening probability in response to a given test potential; this persists for several seconds after repolarization. It has been reported that prepulse facilitation occurs via dissociation of the guanosine triphosphate (GTP)-binding proteins (G-proteins) from the VDCCs and that recovery from facilitation involves rebinding of the G-proteins. The heterotrimeric G-proteins act as switches that regulate information processing circuits connecting cell surface G-protein-coupled-receptors to a variety of effectors. In this study, we have studied the characterization of G-protein subtypes in prepulse facilitation of VDCCs currents (Ica) in hamster submandibular ganglion (SMG) neurons, using whole-cell patch clamp recordings. Under control conditions, with GTP (0.1 mM) in the recording pipette, the rate of prepulse facilitation was 19.0 +/- 1.9% (n = 13). Intracellular dialysis with GDP-beta-S (0.1 mM), G-protein blocker, and pretreatment of neurons with N-ethylmaleimide (NEM) (100 microM for 2 min), Gi/o blocker, attenuated the rate of prepulse facilitation. Intracellular dialysis of anti-Gq/11-antibody did not alter it. These results suggest that prepulse facilitation of VDCCs is due to Gi/o-types of G-protein, but not to the Gq/11-type, in SMG neurons.

Distinct roles for GFRalpha1 and GFRalpha2 signalling in different cranial parasympathetic ganglia in vivo.

Neurturin (NRTN), signalling via the GDNF family receptor alpha2 (GFRalpha2) and Ret tyrosine kinase, has recently been identified as an essential target-derived factor for many parasympathetic neurons. NRTN is expressed in salivary and lacrimal glands, while GFRalpha2 and Ret are expressed in the corresponding submandibular, otic and sphenopalatine ganglia. Here, we have characterized in more detail the role of GDNF and NRTN signalling in the development of cranial parasympathetic neurons and their target innervation. Gfra1 mRNA was expressed at E12 but not in newborn cranial parasympathetic ganglia, while Gfra2 mRNA and protein were strongly expressed in newborn and adult cranial parasympathetic neurons and their projections, respectively. In newborn GFRalpha1- or Ret-deficient mice, where many submandibular ganglion neurons were still present, the otic and sphenopalatine ganglia were completely missing. In contrast, in newborn GFRalpha2-deficient mice, most neurons in all these ganglia were present. In these mice, the loss and atrophy of the submandibular and otic neurons were amplified postnatally, accompanied by complete loss of innervation in some target regions and preservation in others. Surprisingly, GFRalpha2-deficient sphenopalatine neurons, whose targets were completely uninnervated, were not reduced in number and only slightly atrophied. Thus, GDNF signalling via GFRalpha1/Ret is essential in the early gangliogenesis of some, but not all, cranial parasympathetic neurons, whereas NRTN signalling through GFRalpha2/Ret is essential for the development and maintenance of parasympathetic target innervation. These results indicate that GDNF and NRTN have distinct functions in developing parasympathetic neurons, and suggest heterogeneity among and within different parasympathetic ganglia.

Synaptic Transmission and Modulation in Submandibular Ganglia. Aspects of a Current-Clamp Study.

The superior salivatory nucleus in the medulla oblongata is the parasympathetic center of the sublingual and the submandibular (SM) glands. The preganglionic axons originating in this parasympathetic center connect postganglionic neurons in the submandibular ganglia. In spite of an earlier electrophysiological study by Langley in 189013), intracellular electrical studies on SM ganglion neurons had not been done because of the technical difficulties in impaling neurons. It was in only 1972 that the authors begun the intracellular electrical studies of SM ganglia in adult rats and hamsters. In this review, we describe the membrane properties of neurons, spontaneous activities of neurons, types of connection between pre- and post-ganglionic neurons, synaptic potentials including fast EPSP, slow IPSP, slow EPSP and slow hyperpolarizing synaptic potential, characteristics of the reflex spike discharges and modulation of synaptic transmission by biogenic substances in SM ganglion neurons. Transfer of information within the ganglia is more complex than simple nicotinic-cholinergic relay, and seems to be specialized for compatibility with the salivary glands. These data reflect the specific characteristics of synaptic transmission in the SM ganglia.

Angiotensin II-induced depolarizations in hamster submandibular ganglion neurons.

Angiotensin II acts as an excitatory neurotransmitter of the sympathetic ganglia. In the parasympathetic neurons, however, angiotensin II (angio II)-induced responses have not been recorded. In this study, we investigated the effects of angio II in the hamster submandibular ganglion (SMG) neurons using a intracellular recording technique. Approximately 70% of these ganglion cells responded with persistent depolarization (3-6 mV, 5-9 min) at a concentration of 10 microM. The angio II-induced depolarizations were caused by the combination of an increase in Na+ conductance and a decrease in K+ conductance. An involvement of K+ channels such as M channels and SK channels in the electrogenesis mechanism was suggested by an inhibitory effect of Ba2+ ion on the component of the increased membrane input resistance during the angio II-induced depolarization. In addition, the angio II-induced depolarizations were mediated through angio II type I (AT1) receptors. Thus angio II is probably a neurotransmitter that increases their excitability in most of the neurons in parasympathetic ganglia.

Inhibition of calcium channels by neurokinin receptor and signal transduction in hamster submandibular ganglion cells

Both substance P (SP) and neurokinin A (NKA) are known as neurotransmitters of the submandibular ganglion (SMG) neurons. SP released from collaterals of the sensory nerves also regulates the excitability of SMG neurons. It has recently been shown that neurokinins (NK) inhibit calcium channels in various neurons. In this study, the effects of NK on voltage-dependent calcium channel current ( I Ca) in SMG cells were investigated using the whole-cell patch-clamp recording method. NK-1 receptor agonist and SP caused inhibition of I Ca in SMG cells in a dose-dependent manner. NK-1 receptor agonist inhibited L-, N- and P/Q-type I Ca components. GDP-β-S included in the pipette solution reduced the NK-1 receptor agonist-induced inhibition of I Ca. In addition, NK-1 receptor agonist-induced inhibition of I Ca was reduced by stimulation of protein kinase C (PKC) but not cyclic AMP-dependent protein kinase (PKA). The results provided evidence for a signal transduction pathway in which calcium channel inhibition by NK receptors required activation of G-protein and PKC-affected step phosphorylation in SMG neurons.