Nicotinic acetylcholine receptors in porcine hypophyseal intermediate lobe cells.

Zhang, Z W; Feltz, P.

doi:10.1113/jphysiol.1990.sp017974

Cited by 43 publications

(35 citation statements)

References 60 publications

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“…In the pig, acetylcholine stimulates the electrical activity of melanotrope cells through activation of typical neuronal-type nAChR (8). In the frog Rana ridibunda, acetylcholine stimulates hormonal secretion and electrical activity of melanotrope cells through activation of Ml muscarinic receptors (9).…”

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confidence: 99%

Functional characterization of a nonclassical nicotine receptor associated with inositolphospholipid breakdown and mobilization of intracellular calcium pools.

Garnier

Lamacz

Tonon

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Classical nicotinic receptors are neurotransmitter-gated channels that, upon activation by acetylcholine, induce the opening of an intrinsic cationic channel. We have recently observed that, in frog pituitary melanotrophs, nicotine stimulates alpha-melanocyte-stimulating hormone (alpha-MSH) release through a noncholinergic mechanism. In the study reported here, we investigated the intracellular events that mediate the response of frog melanotrophs to nicotine. Nicotine was capable of stimulating alpha-MSH release in the absence of Ca2+ and/or Na+ in the extracellular medium. A short pulse of nicotine induced a rapid and transient increase of cytosolic free Ca2+ concentration ([Ca2+]i). The effect of nicotine on Ca2+ mobilization was not affected in the absence of Na+ and Ca2+ in the extracellular medium, indicating that the nicotine-evoked increase in [Ca2+]i did not result from Na+ or Ca2+ influx. Nicotine induced both an increase in inositol trisphosphate and a reduction in phosphaditylinositol bisphosphate concentrations but did not affect cAMP production. The present results indicate that nicotine-induced stimulation of alpha-MSH release in frog melanotrophs can be explained by activation of inositolphospholipid breakdown and mobilization of inositol triphosphate-dependent intracellular Ca2+ pools. These data provide evidence for the existence of an unusual type of noncholinergic nicotine receptor positively coupled to phospholipase C.

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mentioning

confidence: 99%

Functional characterization of a nonclassical nicotine receptor associated with inositolphospholipid breakdown and mobilization of intracellular calcium pools.

Garnier

Lamacz

Tonon

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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“…2). The observation that the removal of divalent cations from the intracellular solution has little effect on the whole-cell I-V relationship has been made for ACh-elicited currents in rat sympathetic ganglion cells (Mathie et al 1987), rat submandibular ganglion cells (Yawo, 1989), rat adrenal chromaffin cells (Hirano et al 1987), rat parasympathetic cardiac ganglion cells (Fieber & Adams, 1991) and porcine intermediate lobe cells (Zhang & Feltz, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Inward rectification of ACh-elicited currents has been reported in mammalian peripheral ganglion cells (Derkach, Selyanko & Skok, 1983;Mathie, Cull-Candy & Colquhoun, 1987;Yawo, 1989;Fieber & Adams, 1991), chromaffin cells (Hirano, Kidokoro & Ohmori, 1987;Maconochie, 1990), and some central nervous system cells (Mulle & Changeux, 1990;Zhang & Feltz, 1990). In addition, macroscopic currents of neuronal nicotinic receptors composed of ac7 or a4 and na subunits reconstituted in Xenopus ooctyes have been reported to be inwardly rectifying (Bertrand, Ballivet & Rungger, 1990;Couturier, Bertrand, Matter, Hernandez, Bertrand, Millar, Valera, Barkas & Ballivet, 1990).…”

Section: Introductionmentioning

confidence: 99%

Inward rectification of acetylcholine‐elicited currents in rat phaeochromocytoma cells.

Ifune

Steinbach

1992

The Journal of Physiology

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“…Acetylcholine-elicited currents of the rat phaeochromocytoma cell line PC12 are inwardly rectifying, as are the ACh-elicited currents of various mammalian peripheral neurons (Derkach, Selyanko & Skok, 1983; Mathie, Cull-Candy & Colquhoun, 1987; MS 1415 Yawo, 1989;Fieber & Adams, 1991), central neurons (Mulle & Changeux, 1990;Zhang & Feltz, 1990) and adrenal chromaffin cells (Hirano, Kidokoro & Ohmori, 1987; Maconochie, 1990;Inoue & Kuriyama, 1991). In PC12 cells, this rectification has been shown to depend on at least three voltage-dependent processes: the channel burst duration, single-channel conductance, and a fast process that closes channels at positive potentials (Ifune & Steinbach, 1990a.…”

Section: Introductionmentioning

confidence: 99%

Modulation of acetylcholine‐elicited currents in clonal rat phaeochromocytoma (PC12) cells by internal polyphosphates.

Ifune

Steinbach

1993

The Journal of Physiology

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SUMMARY1. Whole-cell voltage clamp techniques were used to examine acetylcholine (ACh)-elicited currents in differentiated cells of the rat phaeochromocytoma cell line, PC 12.2. In the absence of intracellular Mg2+, the whole-cell current-voltage relationship for the ACh-elicited current displayed inward rectification which was reduced in part by the presence of 5 mm internal adenosine 5'-triphosphate (ATP).3. The reduction in the rectification attributed to ATP developed over the first 15-20 min of whole-cell recording. Similar results were obtained with a non-hydrolysable ATP analogue, adenosine-5'-0-3-thiotriphosphate (ATPyS), or cytosine 5'-triphosphate (CTP) in the internal solution, but not with adenosine 5'-diphosphate (ADP) or pyrophosphate.4. The magnitude of the ACh-elicited current was also dependent on recording time and the composition of the internal pipette solution. The magnitude of the peak ACh-elicited current increased over time when the cell was internally perfused with the control solution or a pipette solution containing pyrophosphate, ATPyS, or ADP. The largest sustained increases in ACh-elicited current were observed in the presence of internal pyrophosphate or ATPyS. In contrast, with internal ATP or CTP, the whole-cell current initially increased, then steadily decreased with recording time.5. The desensitization rate of the ACh-elicited current increased with recording time irrespective of the composition of the intracellular solution.6. The actions of the compounds tested make it likely that the changes in the whole-cell current-voltage relationship, peak current, and desensitization are produced by separate mechanisms. The mechanisms underlying these changes are unknown, but the ability of the compounds to chelate divalent cations is unlikely to be the explanation. Other unlikely explanations include phosphorylation of the ACh receptor or regulation by GTP-binding proteins.

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Nicotinic acetylcholine receptors in porcine hypophyseal intermediate lobe cells.

Cited by 43 publications

References 60 publications

Functional characterization of a nonclassical nicotine receptor associated with inositolphospholipid breakdown and mobilization of intracellular calcium pools.

Functional characterization of a nonclassical nicotine receptor associated with inositolphospholipid breakdown and mobilization of intracellular calcium pools.

Inward rectification of acetylcholine‐elicited currents in rat phaeochromocytoma cells.

Modulation of acetylcholine‐elicited currents in clonal rat phaeochromocytoma (PC12) cells by internal polyphosphates.

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