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Showing papers on "Arecoline published in 1979"


Journal ArticleDOI
TL;DR: Rat cerebellar cyclic guanosine 3′,5′-monophosphate cGMP concentrations were determined by radioimmune methods after sacrifice with focused microwave fixation in animals pretreated with ethanol, arecoline, atropine and nicotine alone and in various combinations, suggesting that ethanol's depressant actions on cerebellars are independent of cholinergic mechanisms.

59 citations


Journal ArticleDOI
TL;DR: It is concluded that the muscarinic receptors present in the s.n. pars reticulata play a role in the control of posture opposite to that of the nigral GABA receptors.

56 citations


Journal ArticleDOI
TL;DR: It is concluded that a noradrenergic--cholinergic interaction of the muscarinic type exists in brain and may have a function in the control of arousal, with catalepsy at one extreme and locomotor stimulation at the other.

13 citations


Journal ArticleDOI
TL;DR: The incorporation of (14C)-leucine into the total proteins of the hippocampus is inhibited by high concentrations of cholinergic agonists, with nicotinic substances being more effective than muscarinic compounds (such as arecoline and pilocarpine).
Abstract: The incorporation of (14C)-leucine into the total proteins of the hippocampus is inhibited by high concentrations of cholinergic agonists, with nicotinic substances (such as 1,1-dimethyl-4-phenyl-piperazine) being more effective than muscarinic compounds (such as arecoline and pilocarpine). Under these conditions the incorporation of (3H)-fucose is not influenced.

3 citations


Journal Article
TL;DR: The results suggest that pilocarpine and arecoline act as ACh-releaser in this tissue and that the ouabain-induced cholinergic potentiation may be attributable to a dual mechanism, facilitation of ACh release at presynaptic site and alteration of the membrane excitability at postsynaptic site.
Abstract: In the guinea-pig vas deferens, the contractions induced by pilocarpine and arecoline, unlike ACh, were markedly reduced by treatment with procaine (10(-6) g/ml) or hemicholinium (5 x 10(-4) g/ml). These reductions by hemicholinium were completely recovered after exposure to choline. The contractile responses to these three agonists were eliminated by atropine (3 x 10(-8) g/ml) but enhanced by neostigmine (3 x 10(-8) g/ml), though these were not affected at all by tetrodotoxin (3 x 10(-8) g/ml) or hexamethonium (10(-5) g/ml). The contractile responses to ACh, pilocarpine and arecoline were potentiated by ouabain (10(-6) g/ml). These potentiations were more marked in pilocarpine and arecoline than those in ACh. The potentiation in response to arecoline was maximal after incubation with ouabain for 5 min but that to ACh for 45 min. The results suggest that pilocarpine and arecoline act as ACh-releaser in this tissue and that the ouabain-induced cholinergic potentiation may be attributable to a dual mechanism, facilitation of ACh release at presynaptic site and alteration of the membrane excitability at postsynaptic site.

2 citations


Journal ArticleDOI
TL;DR: Experiments on unanesthetized rats showed that the hyperthermic effect of prostaglandin E2 (PG-E2) is not prevented by aspirin, but can be considerably weakened by injection of arecoline, noradrenalin, serotonin, histamine, and CaCl2 into the lateral ventricles of the brain or by intraperitoneal injection of eserine.
Abstract: Experiments on unanesthetized rats showed that the hyperthermic effect of prostaglandin E2 (PG-E2) is not prevented by aspirin, but can be considerably weakened by injection of arecoline, noradrenalin, serotonin, histamine, and CaCl2 into the lateral ventricles of the brain or by intraperitoneal injection of eserine. Experiments on unanesthetized rabbits showed that arecoline and nicotine have a similar action on PG-E2-induced hyperthermia if injected into the 3rd ventricle. Effects of serotonin and arecoline also were found when reinjected into the cerebral ventricles. In the center for heat loss there are evidently mechanisms which incorporate cholinergic neurons whose activity is not totally inhibited by prostaglandins.

2 citations


Journal ArticleDOI

1 citations


Book ChapterDOI
01 Jan 1979
TL;DR: It is concluded that there exists a noradrenergic-cholinergic (muscarinic) interaction in the central nervous system which is involved in the control of motor activity.
Abstract: Catalepsy produced by the cholinergic (ACh) agonists, arecoline and pilocarpine, was blocked in rats in which the ascending noradrenergic (NA) projections had been selectively destroyed by intracerebral injections of 6-hydroxydopamine (6-OHDA). The same lesions potentiated the motor stimulant effects of the anticholinergic drugs, scopolamine and atropine. It is concluded that there exists a noradrenergic-cholinergic (muscarinic) interaction in the central nervous system which is involved in the control of motor activity.