Acetylcholine and slow synaptic inhibition in frog sympathetic ganglion cells

Weight, Forrest F.; Padjen, Ante L.

doi:10.1016/0006-8993(73)90506-4

Cited by 75 publications

(27 citation statements)

References 11 publications

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“…3 and 5) that occurs during the ACh-evoked inhibition of cells of the nucleus reticularis but not during inhibition of the same cells to a similar degree by GABA and glycine could be regarded as tentative evidence for the view that changes in ionic conductance evoked by ACh must differ from the large increases in chloride conductance that have been shown to be associated with the actions of GABA (Dreifuss, Kelly & Krnjevic, 1969) and glycine (Ten Bruggencate & Engberg, 1971). Although the rapid onset of the ACh-evoked inhibition on cells of the nucleus reticularis is quite unlike the slow onset of the ACh-evoked inhibition of frog ganglion cells described by Weight & Padjen (1973), the high firing rate of the neurones in the nucleus reticularis could be the result of an abnormally high Na+ permeability and in this situation even small reductions in Na+ permeability could cause the immediate onset of inhibition. Indeed Krnjevic (1974) Photomicrographs from four different experiments in which subsequent histological analysis showed the micro-electrode tracks to have penetrated the nucleus reticularis.…”

Section: /12mentioning

confidence: 73%

“…On the other hand the atropine sensitive hyperpolarizing action of ACh on neuroblastoma cells in tissue culture (Nelson, Peacock & Amano, 1971;Nelson & Peacock, 1972) and on C-cells of the frog sympathetic ganglion (Weight & Padjen, 1973) is associated with an increase in membrane resistance that may well be mediated by a decrease in sodium conductance. No clear change in membrane potential or permeability has been observed during the initial depressant action of ACh on cortical neurones (Krnjevic, Pumain & Renaud, 1971).…”

Section: /12mentioning

confidence: 99%

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Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Ben-Ari¹,

Dingledine²,

Kanazawa³

et al. 1976

The Journal of Physiology

136

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SUMMARY1. Short iontophoretic pulses of acetylcholine (ACh) inhibited almost every spontaneously active cell encountered in the nucleus reticularis thalami of cats anaesthetized with a mixture of halothane, nitrous oxide and oxygen. On 200 cells the mean current needed to eject an effective inhibitory dose of ACh was 67 + 2 nA. When the ACh-evoked inhibition was mimicked by y-aminobutyric acid (GABA) or glycine on the same cell, the current required to release ACh was found to be approximately twice as great as that required to release an equally effective dose of GABA or glycine.2. The ACh inhibitions developed with a latency which was very much shorter than that for ACh excitation in cells of the ventrobasal complex. The latency of the ACh-evoked inhibition was as rapid as the onset and offset of the excitation of the same cells by glutamate and their inhibition by GABA or glycine.3. The firing pattern of ACh-inhibited neurones in the nucleus reticularis was characterized by periods of prolonged, high frequency bursts, and their mean firing frequency was 22 Hz. Raster dot displays and interspike interval histograms showed that whereas ACh suppressed the spikes that occurred between bursts much more readily than those that occurred during bursts, all spikes were equally sensitive to the depressant action of GABA and glycine. Large doses of ACh provoked or exaggerated burst activity.4. ACh-evoked inhibition was extremely sensitive to blockade by short iontophoretic applications of atropine, which had no effect on the inhibitions evoked on the same cell by equipotent doses of GABA or glycine. The Y. BEN-ARI AND OTHERSACh-evoked inhibitions were also antagonized by dihydro-fl-erythroidine released with slightly larger currents. When tested on the same cell, small iontophoretic applications of picrotoxin and bicuculline methoiodide blocked the inhibition evoked by GABA but had no effect on that evoked by ACh. Iontophoretic strychnine only rarely affected the inhibition evoked by ACh, while readily blocking the inhibition evoked on the same cell by an equipotent dose of glycine. In two cats, intravenous strychnine (1.2 mg/kg) had no effect on the ACh-evoked inhibition, while greatly reducing the sensitivity of the cell under study to glycine.5

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Section: /12mentioning

confidence: 73%

Section: /12mentioning

confidence: 99%

Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Ben-Ari¹,

Dingledine²,

Kanazawa³

et al. 1976

The Journal of Physiology

136

View full text Add to dashboard Cite

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“…In rabbit ganglia the hyperpolarization has been attributed to the release of a catecholamine (Libet, 1970); in amphibia, on the other hand, this effect is direct (Weight & Padjen, 1973;Hartzell et al, 1977). In the rat isolated ganglion evidence for an indirect, catecholamine-mediated effect was equivocal.…”

Section: Agonistsmentioning

confidence: 99%

Muscarinic Receptors in Rat Sympathetic Ganglia

Brown

Fatherazi

Garthwaite

et al. 1980

British J Pharmacology

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I Potential changes in isolated superior cervical ganglia of the rat produced by muscarinic-receptor agonists were recorded by an extracellular 'air-gap' method. Depolarization was accompanied by facilitation of submaximal ganglionic transmission. 6 Muscarine (1 to 100 gM) initially reduced, then increased, the rate of 86Rb+-efflux from isolated ganglia at both 6 and 120 mM [K ]. These effects were reduced by 1 AM hyoscine.7 No consistent change in the amounts of cyclic 3',5'-guanosine monophosphate in isolated ganglia accompanying muscarinic depolarization could be detected.8 Mean against ED5o values (pM) for contracting the rat isolated ileum were: oxotremorine 0.012, methylfurmethide 0.29, (±)muscarine 0.48, pilocarpine 7.8 and AHR-602 9.9. Mean antagonist K, values (nM) were: hyoscine 0.17, atropine 0.34 and lachesine 0.27. 9 It is concluded that ganglionic muscarinic receptors are quite similar to ileal receptors in terms of agonist ED50 and antagonist K, values, and that the major difference between them lies in the greater 'efficacy' of certain agonists (pilocarpine, AHR-602 and McN-A-343) on the ganglion.

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“…The pharmacology of the depolarizing response has been studied in detail (Brown et al, 1980a,b), but that ofthe smaller hyperpolarization has received less attention. The purpose of our experiments was to compare the pharmacology of the two potentials and to examine the possible involvement of catecholamines in the mediation ofthe hyperpolarizing response (see Weight & Padjen, 1973;Cole & Shinnick-Gallagher, 1980;Ivanov & Skok, 1980;Ashe & Libet, 1982;Rafuse & Smith, 1986). A preliminary account of some of this work has been published (Newberry et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological differences between two muscarinic responses of the rat superior cervical ganglion in vitro

Newberry

Priestley

1987

British J Pharmacology

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1Pharmacological differences have been observed between the muscarinic agonist-induced depolarizing and hyperpolarizing responses of the rat isolated superior cervical ganglion. 2 Pirenzepine (0.3 AM) selectively reduced the depolarizing response and unmasked the hyperpolarizing response. No such selectivity was observed with a concentration of N-methylatropine which was equipotent with pirenzepine in antagonizing the depolarizing response. 3 The neuromuscular blocking agents gallamine (1O tM) and pancuronium (3 jM) exhibited the oppositive selectivity to pirenzepine, both dramatically reduced the hyperpolarization but only slightly antagonized the depolarization. 4 The potencies of a range ofagonists in evoking the depolarizing and hyperpolarizing responses, the latter in the presence of 0.3 tAM pirenzepine, have been determined. Methylfurmethide failed to hyperpolarize the ganglion at concentrations which evoked maximal depolarizations. 5 The muscannic hyperpolarization did not appear to be mediated by the secondary release of catecholamines. 6 It was concluded that the two muscarinic responses on the rat superior cervical ganglion, the slow depolarization and faster hyperpolarization, are mediated by different muscarinic receptor subtypes.

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Acetylcholine and slow synaptic inhibition in frog sympathetic ganglion cells

Cited by 75 publications

References 11 publications

Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Inhibitory effects of acetylcholine on neurones in the feline nucleus reticularis thalami.

Muscarinic Receptors in Rat Sympathetic Ganglia

Pharmacological differences between two muscarinic responses of the rat superior cervical ganglion in vitro

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