effect of acetylcholine on the electrical and secretory activities of frog pituitary melanotrophs

Louiset, Estelle; Cazin, L.; Duval, Olivier; Lamacz, Marek; Tonon, Marie Christine; Vaudry, Hubert

doi:10.1016/0006-8993(90)91353-i

Cited by 21 publications

(10 citation statements)

References 42 publications

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“…In the frog Rana ridibunda, acetylcholine stimulates hormonal secretion and electrical activity of melanotrope cells through activation of Ml muscarinic receptors (9). In this latter species, nicotine also appears to be a potent stimulator of a-melanocyte-stimulating hormone (a-MSH) release and spiking activity (10), but the effect of nicotine is neither mimicked by nicotinic cholinergic agonists nor blocked by nicotinic antagonists (10), suggesting that the action of nicotine on frog melanotrope cells is mediated by a nonclassical nicotine receptor, which might be related to the noncholinergic nicotinic binding site characterized by Abood et al (6) in the rat brain.…”

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confidence: 99%

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RETRACTED: 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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“…In contrast, incubation offrog NILs with 10 ,uM nicotine had no effect on cAMP production (data not shown). (10). In the present study, we have investigated the transduction pathways that are responsible for the action of nicotine on this previously unreported type of receptor.…”

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confidence: 99%

RETRACTED: 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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“…The bioelectrical activity of melanotrophs is held responsible for the secretion of a-MSH (Tomiko, Taraskevich & Douglas, 1984) since the neuroendocrine factors which increase or decrease the frequency of action potentials respectively stimulate or inhibit a-MSH release (Louiset et al 1989;Louiset, Cazin, Duval, Lamacz, Tonon & Vaudry, 1990;Chartrel, Conlon, Danger, Fournier, Tonon & Vaudry, 1991;Desrues, Lamacz, Jenks, Vaudry & Tonon, 1993;Valentijn, Vaudry, Kloas & Cazin, 1994). We have recently shown that adenosine is a potent inhibitor of both bioelectrical activity and a-MSH secretion in frog melanotrophs (Chartrel et al 1992;).…”

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confidence: 99%

A‐type potassium current modulated by A1 adenosine receptor in frog melanotrophs.

Mei

Louiset

Vaudry

et al. 1995

The Journal of Physiology

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1. Transient outward current was recorded in cultured frog melanotrophs with the whole‐cell configuration of the patch‐clamp technique. The ionic dependence, kinetics and pharmacological properties of the current were studied. The effects of the A1 adenosine receptor agonist R‐N6‐phenylisopropyl‐adenosine (R‐PIA) on this current were also investigated. 2. In tetrodotoxin‐ and cobalt‐containing solution, depolarization from ‐120 mV elicited both transient and delayed outward currents. Pulses from ‐60 mV activated only a sustained late current. 3. 4‐Aminopyridine (4 mM) reduced the transient outward current much more than the delayed outward current. In contrast, tetraethylammonium (10‐20 mM) selectively reduced the delayed current. 4. Tail current measurements showed a positive shift in the reversal potential when external K+ concentration was increased, indicating that K+ was the predominant charge carrier. 5. Steady‐state inactivation was complete at potentials positive to ‐10 mV and removed by hyperpolarization. 6. Inactivation of the transient current was slowed and accelerated in oxidizing and reducing conditions, respectively, confirming the involvement of an inactivating ‘ball and chain’ peptide. 7. R‐PIA increased the transient current. The steady‐state inactivation curve was shifted towards more positive potentials without changing the activation kinetics. Pretreatment with pertussis toxin (1 microgram ml‐1) blocked the response to R‐PIA. 8. It is concluded that frog melanotrophs possess an A‐type current that is likely to play an important role in excitability. This current, which is directly modulated by A1 adenosine receptors through a Gi/G(o) protein, appears to be responsible for the inhibitory effects of adenosine on electrical activity.

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“…Melantrophs of the frog pars intermedia exhibit spontaneous action potentials in very much the same way as neurones (Louiset, Cazin, Lamacz, Tonon & Vaudry, 1988) and the action of hypothalamic factors on the electrical and secretory activities of those cells is strictly correlated (Louiset, Cazin, Lamacz, Tonon & Vaudry, 1989;Louiset, Cazin, Duval, Lamacz, Tonon & Vaudry, 1990a;Louiset et al 1990b;Valentijn, Louiset, Vaudry & Cazin, 1991a;Valentijn, Vaudry & Cazin, 1993a;Valentijn, Vaudry, Kloas & Cazin, 1994). Since the frog pars intermedia is composed of a homogeneous population of endocrine cells, it provides a valuable model system in which to investigate the mechanism of action of various neurotransmitters on electrical activity.…”

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Inhibitory effect of adenosine on electrical activity of frog melanotrophs mediated through A1 purinergic receptors.

Mei

Vaudry

Cazin

1994

The Journal of Physiology

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1. The effects of adenosine were studied in cultured frog melanotrophs by the patch-clamp technique.2. In cell-attached experiments, most cells responded to adenosine (50 /M) by a reversible inhibition of action current discharges without any apparent desensitization. 3. In whole-cell experiments, adenosine provoked a hyperpolarization accompanied by a depression of spontaneous action potentials and a decrease in membrane resistance. When adenosine was repeatedly applied, tachyphylaxis was observed. Addition of GTP (100 /M) in the intracellular solution augmented the percentage of cells hyperpolarized by adenosine, and the duration and amplitude of the hyperpolarization, and prevented the tachyphylaxis.4. Pretreatment with pertussis toxin (1 jug ml-') blocked adenosine-induced inhibition.5. In cells dialysed with the non-hydrolysable GTP analogue GTPyS (100 SM), adenosine caused a sustained, strong hyperpolarization and an irreversible inhibition of spikes. 6. The effect of adenosine was mimicked by the A1 receptor agonist R-PIA (R -N6-phenylisopropyl-adenosine; 50/uM) and blocked by the A1 receptor antagonist CPDPX (8-cyclopentyl-1,3-dipropylxanthine, 50/uM). The A2 receptor antagonist CGS15943 (9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolo[1,5-c] quinazoline-5-imine; 50/uM) did not affect the adenosine-induced response.7. The results suggest that, in frog melanotrophs, adenosine exerts a direct hyperpolarizing effect accompanied by blockage of spontaneous action potentials. The effect of adenosine is mediated through A1 receptors coupled to a Gi/o protein.

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effect of acetylcholine on the electrical and secretory activities of frog pituitary melanotrophs

Cited by 21 publications

References 42 publications

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

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

A‐type potassium current modulated by A1 adenosine receptor in frog melanotrophs.

Inhibitory effect of adenosine on electrical activity of frog melanotrophs mediated through A1 purinergic receptors.

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