Contribution of nicotinic and muscarinic receptors in the secretion of catecholamines evoked by endogenous and exogenous acetylcholine

Wakade, Arun R.; Wakade, Taruna D.

doi:10.1016/0306-4522(83)90235-x

Cited by 149 publications

(84 citation statements)

References 21 publications

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“…magnitude of the [Ca 2ϩ ] i elevations produced by mAChR activation is less than that produced by influx, the elevation produced by mAChR activation persists much longer and seems to affect a significantly greater portion of the chromaffin cell membrane. Based on estimates of the Ca 2ϩ dependence of exocytosis from bovine chromaffin cells (Knight and Baker, 1982;Augustine and Neher, 1992b) indicating that secretion can be initiated at [Ca 2ϩ ] i lower than 1 M, our results are consistent with previous reports implicating mAChRs in eliciting secretion in rat chromaffin cells (Wakade and Wakade, 1983;Malhotra et al, 1988). This contrasts with bovine chromaffin cells, in which release of Ca 2ϩ from intracellular stores by mAChR activation produces relatively weak elevations in [Ca 2ϩ ] i O'Sullivan et al, 1989) and is ineffective in producing secretion (Fisher et al, 1981;Kim and Westhead, 1989).…”

Section: Implications For Secretionsupporting

confidence: 91%

[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells

1996

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Submembrane [Ca 2ϩ ] i changes were examined in rat chromaffin cells by monitoring the activity of an endogenous Ca 2ϩ -dependent protein: the large conductance Ca 2ϩ -and voltageactivated K ϩ channel (also known as the BK channel). The Ca 2ϩ and voltage dependence of BK current inactivation and conductance were calibrated first by using defined [Ca 2ϩ ] i salines. This information was used to examine submembrane [Ca 2ϩ ] i elevations arising out of Ca 2ϩ influx and muscarine-mediated release of Ca 2ϩ from intracellular stores. During Ca 2ϩ influx, some BK channels are exposed to [Ca 2ϩ ] i of at least 60 M. However, the distribution of this [Ca 2ϩ ] i elevation is highly nonuniform so that the average [Ca 2ϩ ] i detected when all BK channels are activated is only ϳ10 M. Intracellular dialysis with 1 mM or higher EGTA spares only the BK channels activated by the highest [Ca 2ϩ ] i during influx, whereas dialysis with 1 mM or higher BAPTA blocks activation of all BK channels. Submembrane [Ca 2ϩ ] i elevations fall rapidly after termination of short (5 msec) Ca 2ϩ influx steps but persist above 1 M for several hundred milliseconds after termination of long (200 msec) influx steps. In contrast to influx, the submembrane [Ca 2ϩ ] i elevations produced by release of intracellular Ca 2ϩ by muscarinic actetylcholine receptor (mAChR) activation are much more uniform and reach peak levels of 3-5 M. Our results suggest that during normal action potential activity only 10 -20% of BK channels in each chromaffin cell see sufficient [Ca 2ϩ ] i to be activated.

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Section: Implications For Secretionsupporting

confidence: 91%

[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells

1996

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“…Table 2). In agreement with previous results (Teraoka et al, 1991) (20 mM (Douglas & Rubin, 1961;Ito et al, 1978;1979;Kilpatrick et al, 1981;Knight & Baker, 1983;Knight & Kesteven, 1983;Wakade & Wakade, 1983). However, the mechanism underlying the depolarization is different between stimulants, ACh and veratridine cause depolarization resulting mainly from the activation of nicotinic receptor channels and voltage-dependent, tetrodotoxin-sensitive Na' channels, respectively.…”

Section: Resultssupporting

confidence: 92%

Inhibitory effects of caffeine on secretagogue‐induced catecholamine secretion from adrenal chromaffin cells of the guinea‐pig

Nakazato

Tani

Sugawara

et al. 1994

British J Pharmacology

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1 The inhibitory action of caffeine on catecholamine secretion induced by secretagogues was investigated in perfused adrenal glands and dispersed chromaffin cells of the guinea-pig. 2 Caffeine (10 mM) caused a reversible inhibition of catecholamine secretion evoked by acetylcholine (ACh, 50 jiM), KCl (56 mM, high K+) and veratridine (100 gtM) and that induced by muscarinic receptor activation in the absence of extracellular Ca2' in perfused adrenal glands.3 In dispersed chromaffin cells, caffeine caused a dose-dependent inhibition of the secretory responses to 100 jiM ACh and veratridine. Forskolin (30 gtM), dibutyryl cyclic AMP (1 mM) and 8-bromo cyclic AMP (1 mM) did not mimic the action of caffeine. 4 In the voltage-clamp, whole-cell recording mode (at a holding potential of -60 mV or -70 mV), ACh (100I1M) evoked an inward current, and depolarizing pulses elicited inward Na+, Ca2" and outward K+ currents. All these responses were partially inhibited by caffeine (20 mM).5 ACh rapidly increased the intracellular concentration of Ca2" ([Ca2+D in fura-2-loaded cells in either the presence or the absence of external Ca2", though its magnitude was decreased by about 50% in Ca2+-free conditions. Caffeine (20 mM) inhibited these ACh-induced increases in [Ca2J]i.6 In permeabilized chromaffin cells, caffeine (20 mM) caused an inhibition of catecholamine secretion evoked by Ca2" (1O pM). 7 These results suggest that caffeine inhibits evoked catecholamine secretion through mechanisms such as the blockade of voltage-dependent Na+ and Ca2+ currents and ACh receptor current, and reduction of the release of intracellularly stored Ca2`and/or Ca2+-sensitivity of the secretory apparatus.

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“…At rat splanchnic nerve-chromaffin cell synapses, postsynaptic nicotinic receptors (nAChRs) dominantly contribute to acetylcholine-mediated excitatory responses and ensuing secretion (Douglas and Rubin, 1961;Wakade and Wakade, 1983). Although most nAChRs contain ␣ and ␤ subunits, some contain only ␣ subunits, as exemplified by ␣7, ␣9, and ␣9/␣10 nAChRs.…”

Section: Introductionmentioning

confidence: 99%

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

Colomer

Olivos-Oré²,

Vincent³

et al. 2010

J. Neurosci.

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An increase in circulating adrenal catecholamine levels constitutes one of the mechanisms whereby organisms cope with stress. Accordingly, stimulus-secretion coupling within the stressed adrenal medullary tissue undergoes persistent remodeling. In particular, cholinergic synaptic neurotransmission between splanchnic nerve terminals and chromaffin cells is upregulated in stressed rats. Since synaptic transmission is mainly supported by activation of postsynaptic neuronal acetylcholine nicotinic receptors (nAChRs), we focused our study on the role of ␣9-containing nAChRs, which have been recently described in chromaffin cells. Taking advantage of their specific blockade by the ␣-conotoxin RgIA (␣-RgIA), we unveil novel functional roles for these receptors in the stimulus-secretion coupling of the medulla. First, we show that in rat acute adrenal slices, ␣9-containing nAChRs codistribute with synaptophysin and significantly contribute to EPSCs. Second, we show that these receptors are involved in the tonic inhibitory control exerted by cholinergic activity on gap junctional coupling between chromaffin cells, as evidenced by an increased Lucifer yellow diffusion within the medulla in ␣-RgIA-treated slices. Third, we unexpectedly found that ␣9-containing nAChRs dominantly (Ͼ70%) contribute to acetylcholine-induced current in cold-stressed rats, whereas ␣3 nAChRs are the main contributing channels in unstressed animals. Consistently, expression levels of ␣9 nAChR transcript and protein are overexpressed in cold-stressed rats. As a functional relevance, we propose that upregulation of ␣9-containing nAChR channels and ensuing dominant contribution in cholinergic signaling may be one of the mechanisms whereby adrenal medullary tissue appropriately adapts to increased splanchnic nerve electrical discharges occurring in stressful situations.

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Contribution of nicotinic and muscarinic receptors in the secretion of catecholamines evoked by endogenous and exogenous acetylcholine

Cited by 149 publications

References 21 publications

[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells

[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells

Inhibitory effects of caffeine on secretagogue‐induced catecholamine secretion from adrenal chromaffin cells of the guinea‐pig

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

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Contribution of nicotinic and muscarinic receptors in the secretion of catecholamines evoked by endogenous and exogenous acetylcholine

Cited by 149 publications

References 21 publications

[Ca2+]iElevations Detected by BK Channels during Ca2+Influx and Muscarine-Mediated Release of Ca2+from Intracellular Stores in Rat Chromaffin Cells

[Ca2+]iElevations Detected by BK Channels during Ca2+Influx and Muscarine-Mediated Release of Ca2+from Intracellular Stores in Rat Chromaffin Cells

Inhibitory effects of caffeine on secretagogue‐induced catecholamine secretion from adrenal chromaffin cells of the guinea‐pig

Functional Characterization of α9-Containing Cholinergic Nicotinic Receptors in the Rat Adrenal Medulla: Implication in Stress-Induced Functional Plasticity

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[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells

[Ca²⁺]_iElevations Detected by BK Channels during Ca²⁺Influx and Muscarine-Mediated Release of Ca²⁺from Intracellular Stores in Rat Chromaffin Cells