Showing papers on "Arecoline published in 1972"
TL;DR: Bilateral injection of atropine into the caudate-putamen and globus pallidus did not modify the catalepsy induced by peripheral administration of haloperidol or arecoline but intranigral atropines markedly potentiated the cataleptic effects of these drugs.
193 citations
Journal Article•
TL;DR: Pilocarpine stimulated the turnover rate of serotonin and approximately doubled the concentrations of acetylcholine, of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and of the dopamine metabolite homovanillic acid, but the drugs also differed in their biochemical effects on neurotransmitters in the brain.
Abstract: Despite the similarities between the peripheral muscarinic actions of pilocarpine and arecoline, the central excitatory effect of pilocarpine HCL (100 mg/kg i.p.) lasted several hours in rats and was accompanied by clonic movementS, whereas the excitation induced by arecoline (50 mg/kg i.p.) lasted only 10 minutes and was associated with tremors. The drugs also differed in their biochemical effects on neurotransmitters in the brain. Pilocarpine stimulated the turnover rate of serotonin and approximately doubled the concentrations of acetylcholine, of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and of the dopamine metabolite homovanillic acid. The changes in acetylcholine and 5-HIAA occurred within 0.5 hour and persisted for at least four hours. Arecoline administration also increased acetylcholine and 5-HIAA levels, but the arecoline-induced rise in acetyleholine occurred within five minutes and returned to normal within 20 minutes, well before the 5-HIAA levels began to rise. Prior administration of atropine sulfate (5 mg/kg i.p.), which blocked the overt behavioral and cholinomimetic actions of both drugs, diminished the arecoline-incluced rises in acetylcholine and 5-HIAA levels. However, atropine failed to prevent the pilocarpine-induced rises in acetylcholine and 5-HIAA levels.
58 citations
TL;DR: A comparison of these results with previous work strongly suggests that the underlying mechanisms involved in the reduction of spontaneous motor activity are not the same as those involving in the production of catalepsy by neuroleptic and cholinergic drugs and therefore opposes the idea that the cataleptic effect of a drug is the extension of its depressant effect upon locomotor activity.
38 citations
TL;DR: The specific cueing effects of these two cholinergic agonists suggests the presence of distinct C.N.S. receptor sites of action for m- and n-cholinergic drugs.
34 citations
TL;DR: The results suggest that the arecoline-produced interoceptive cue is of central origin, and the possible existence of specific muscarinic and nicotinic cholinergic receltors in the CNS is discussed.
15 citations
TL;DR: It is suggested that arecoline and pilocarpine increase brain acetylcholine levels by different mechanisms, and the mechanism by which these drugs raise the brain acetolcholine level is elucidated.
Abstract: TREATMENT of mice with arecoline or oxotremorine produces tremors accompanied by a transient increase in the brain level of acetylcholine lasting for 20 to 30 min1. We reported that administration of pilocarpine, whose peripheral cholinomimetic effects resemble those of arecoline, also markedly increases the level of brain acetylcholine in rats2,3. By contrast with other cholinomimetics, however, the pilocarpine-induced increase in acetylcholine lasts for several hours and is not accompanied by tremors. These findings suggest that arecoline and pilocarpine increase brain acetylcholine levels by different mechanisms. This study compares the effects of arecoline and pilocarpine administration on the conversion of choline-3H to acetylcholine-3H to elucidate the mechanism by which these drugs raise the brain acetylcholine level.
12 citations