Neuronal Nicotinic Acetylcholine Receptors on Bovine Chromaffin Cells: Cloning, Expression, and Genomic Organization of Receptor Subunits

Campos‐Caro, Antonio; Smillie, F. I.; Toro, Eduardo Domı́nguez del; Rovira, José Carlos; Vicente-Agullo, Francisco; Chapuli, J.; Juı́z, José M.; Sala, Salvador; Sala, Francisco; Ballesta, Juan J.; Criado, Manuel

doi:10.1046/j.1471-4159.1997.68020488.x

Cited by 123 publications

(82 citation statements)

References 33 publications

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“…By contrast, in unstressed rats, ␣9-containing nAChRs contribute to a lesser extent to ACh-evoked current, the major contribution being that of ␣3 nAChRs, consistent with a dominant expression of ␣3/␤4 nAChRs in chromaffin cells (Criado et al, 1992;Campos-Caro et al, 1997;Sala et al, 2008). We propose that under resting conditions, in which expression level of ␣9 subunit is low, the synaptic response of chromaffin cells would be dominated by ␣3 subunit-containing nAChRs (Barbara and Takeda, 1996;Martin et al, 2003Martin et al, , 2005 that exhibit low Ca 2ϩ permeability (Fucile, 2004).…”

Section: Dominant Expression and Function Of ␣9-containing Nachrs In mentioning

confidence: 54%

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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Section: Dominant Expression and Function Of ␣9-containing Nachrs In mentioning

confidence: 54%

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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“…Although many nicotinic acetylcholine receptor subunits are expressed in the central and peripheral nervous systems, the distributions of α3β4 nicotinic acetylcholine receptor are mainly restricted to several tissues such as adrenal chromaffin cells [8,9]. The α3β4 nicotinic acetylcholine receptors play an important role for release of catecholamine releases [10].…”

Section: Introductionmentioning

confidence: 99%

Quercetin Inhibits α3β4 Nicotinic Acetylcholine Receptor-Mediated Ion Currents Expressed inXenopusOocytes

Lee

Hwang

Choi

et al. 2011

Korean J Physiol Pharmacol

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Quercetin mainly exists in the skin of colored fruits and vegetables as one of flavonoids. Recent studies show that quercetin, like other flavonoids, has diverse pharmacological actions. However, relatively little is known about quercetin effects in the regulations of ligand-gated ion channels. In the previous reports, we have shown that quercetin regulates subsets of homomeric ligand-gated ion channels such as glycine, 5-HT3A and α 7 nicotinic acetylcholine receptors. In the present study, we examined quercetin effects on heteromeric neuronal α 3β 4 nicotinic acetylcholine receptor channel activity expressed in Xenopus oocytes after injection of cRNA encoding bovine neuronal α 3 and β 4 subunits. Treatment with acetylcholine elicited an inward peak current (IACh) in oocytes expressing α 3β 4 nicotinic acetylcholine receptor. Co-treatment with quercetin and acetylcholine inhibited IACh in oocytes expressing α 3β 4 nicotinic acetylcholine receptors. The inhibition of IACh by quercetin was reversible and concentration-dependent. The half-inhibitory concentration (IC50) of quercetin was 14.9± 0.8 μ M in oocytes expressing α 3β 4 nicotinic acetylcholine receptor. The inhibition of IACh by quercetin was voltage-independent and non-competitive. These results indicate that quercetin might regulate α 3β 4 nicotinic acetylcholine receptor and this regulation might be one of the pharmacological actions of quercetin in nervous systems.

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“…Additionally, the previous experiments did not provide information concerning the subtype of nAChR preferentially blocked by catestatin. This is an important issue, because at least two different classes of nAChRs, most likely formed by the combination of ␣ 3 and ␤ 4 subunits or ␣ 7 subunits that bind ␣-bungarotoxin, have been implicated in the control of catecholamine secretion in chromaffin cells (Criado et al, 1992;Campos-Caro et al, 1997;López et al, 1998).…”

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confidence: 99%

Modulatory Mechanism of the Endogenous Peptide Catestatin on Neuronal Nicotinic Acetylcholine Receptors and Exocytosis

et al. 2002

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The catestatin fragment of chromogranin A is the first known endogenous compound able to inhibit catecholamine release elicited by the activation of neuronal nicotinic acetylcholine receptors (nAChRs) of different animal species and catecholaminergic cell types. However, how catestatin regulates the receptor activity, which subunit combination of the heteropentameric forms of receptor is better blocked by the peptide, or how it affects the different stages of the exocytotic process have not yet been evaluated. To address these questions, we have assayed the effects of catestatin: (first) on the inward currents elicited by ACh (I ACh ) in voltage-clamped oocytes expressing different combinations of nAChR subunits; and (second) on the cytosolic Ca 2ϩ concentration, [Ca 2ϩ ] c , and quantal release of catecholamines simultaneously monitored in single adrenal chromaffin cells stimulated with ACh. Catestatin potently blocks all the subtypes of nAChRs studied. Furthermore, it inhibits the ␣ 3 ␤ 4 current in a reversible, noncompetitive, voltage-, and use-dependent manner, a behavior compatible with open-channel blockade. In fura-2-loaded single chromaffin cells, the peptide reduced the [Ca 2ϩ ] c signal and the total release of catecholamines elicited by ACh; however, catestatin did not modify the kinetics or the last step of the exocytotic process. Our results suggest that catestatin might play an autocrine regulatory role in neuroendocrine secretion through its interaction with different native nAChR subtypes; the extent of receptor blockade by the peptide could be acutely regulated by the intensity and duration of the presynaptic stimulus.

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Neuronal Nicotinic Acetylcholine Receptors on Bovine Chromaffin Cells: Cloning, Expression, and Genomic Organization of Receptor Subunits

Cited by 123 publications

References 33 publications

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

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

Quercetin Inhibits α3β4 Nicotinic Acetylcholine Receptor-Mediated Ion Currents Expressed inXenopusOocytes

Modulatory Mechanism of the Endogenous Peptide Catestatin on Neuronal Nicotinic Acetylcholine Receptors and Exocytosis

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