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

Ikegami, Hideaki; Endoh, Takayuki; Suzuki, Takashi

doi:10.1016/s0168-0102(01)00279-6

Cited by 10 publications

(7 citation statements)

References 22 publications

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“…In SMG neurons, we previously demonstrated that several different neurotransmitters produce modulation of VDCCs via a pathway using G-proteins 20,38) . GPCR activated by neurotransmitters couple to the carboxy-terminals of G-protein ␣ subunits, and polyclonal antibodies raised against C-terminal peptide sequences of different G␣ subunits have been shown to functionally antagonize neurotransmitter modulation of VDCCs (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…SMG neurons from hamsters were acutely dissociated with a modified version of the method described previously 20) . In brief, SMG neurons were isolated from 4-6-week-old hamsters and maintained in Ca ‫ם2‬ -free Krebs solution of the following composition (in mM): 136 NaCl, 5 KCl, 3 MgCl 2 ·6H 2 O, 10.9 glucose, 11.9 NaHCO 3 , and 1.1 NaH 2 PO 4 ·2H 2 O.…”

Section: Methodsmentioning

confidence: 99%

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Decay in Prepulse Facilitation of Calcium Channel Currents by Gi/o-Protein Attenuation in Hamster Submandibular Ganglion Neurons, But Not Gq/11.

Endoh

Abe

Suzuki

2001

Bull. Tokyo Dent. Coll.

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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 (I Ca ) in hamster submandibular ganglion (SMG) neurons, using whole-cell patch clamp recordings.Under control conditions, with GTP (0.1mM) in the recording pipette, the rate of prepulse facilitation was ‫%9.1ע0.91‬ (n‫.)31ס‬ Intracellular dialysis with GDP-␤-S (0.1mM), G-protein blocker, and pretreatment of neurons with N-ethylmaleimide (NEM) (100M for 2min), G i/o blocker, attenuated the rate of prepulse facilitation. Intracellular dialysis of anti-G q/11 -antibody did not alter it. These results suggest that prepulse facilitation of VDCCs is due to G i/o -types of G-protein, but not to the G q/11 -type, in SMG neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Decay in Prepulse Facilitation of Calcium Channel Currents by Gi/o-Protein Attenuation in Hamster Submandibular Ganglion Neurons, But Not Gq/11.

Endoh

Abe

Suzuki

2001

Bull. Tokyo Dent. Coll.

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“…The animals were treated in accordance with the principles approved by the Council of the Physiological Society of Japan and in compliance with the guidelines of the Japanese Government. SMG neurons from hamsters were acutely dissociated using a modified version of the methods described previously 15 . In Brief, male hamsters 4-6 weeks old were anesthetized with pentobarbital sodium (30 mg/kg, i.p.)…”

Section: Cell Preparationmentioning

confidence: 99%

“…2B, selective antagonists were applied prior to ADM and CGRP. In contrast to SQ22536 and PKI (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24), in neurons treated with U-73122 (a membrane-permeable aminosteroid which blocks phosphatidylinositol-specific PLC, 10 μM for 15 min), GF109203X (a selective PKC inhibitor, 10 μM for 30 min) and PD98,059 (a MAPK tyrosine kinase inhibitor, 10 μM for 2 min) did not attenuate the ADM-and CGRP-induced facilitation of IBa. These results suggest that ADM and CGRP facilitates VDCCs involving AC and PKA pathways in the SMG neurons (Fig.…”

Section: Pharmacological Characterization Of Cgrp-and Adm-induced Facmentioning

confidence: 99%

Calcitonin gene-related peptide- and adrenomedullin-induced facilitation of calcium current in submandibular ganglion

Endoh

Shibukawa

Tsumura

et al. 2011

Archives of Oral Biology

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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 (ICa) 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 ICa. These facilitations were attenuated by intracellular dialysis of the anti-G α s-protein and pretreatment of SQ22536 (an adenylate cyclase inhibitor).Conclusions: ADM and CGRP facilitates VDCCs mediated by G α s-protein and adenylate cyclase in SMG.3

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“…1 In particular, the acute effect of AngII on L-type calcium currents has been shown to be dependent on the cell type: while in smooth muscle is accepted that AngII induce activation of L-type calcium current; [2][3][4] in neurons and kidney the opposing effect (inhibition of L-type calcium current) is observed. [5][6][7] On the other hand, the effect of this hormone in cardiac muscle is still controversial as AngII was reported to induce an increase 8,9 or a decrease 10,11 of L-type calcium current in heart cells. Although the reason for this disagreement is not known, it is proposed that the experimental approach is relevant.…”

Section: Introductionmentioning

confidence: 99%

L-type calcium channel β subunit modulates angiotensin II responses in cardiomyocytes

Hermosilla

Moreno²,

Itfinca³

et al. 2011

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

Cited by 10 publications

References 22 publications

Decay in Prepulse Facilitation of Calcium Channel Currents by Gi/o-Protein Attenuation in Hamster Submandibular Ganglion Neurons, But Not Gq/11.

Decay in Prepulse Facilitation of Calcium Channel Currents by Gi/o-Protein Attenuation in Hamster Submandibular Ganglion Neurons, But Not Gq/11.

Calcitonin gene-related peptide- and adrenomedullin-induced facilitation of calcium current in submandibular ganglion

L-type calcium channel β subunit modulates angiotensin II responses in cardiomyocytes

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