Drugs online research references
Neurosci Lett. 1989 Apr 24;99(1-2):191-6.
Disruption of muscarinic receptor-G protein coupling is a general property of liquid volatile anesthetics.
Anthony BL, Dennison RL, Aronstam RS.
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912.
The influences of 3 volatile anesthetics, chloroform, enflurane and isoflurane, on muscarinic acetylcholine receptors in rat brainstem were determined. Each of the volatile anesthetics increased [3H]methylscopolamine [( 3H]MS) binding affinity, but did not affect the number of [3H]MS binding sites. Carbamylcholine affinity for brainstem muscarinic receptors was not altered after equilibration of brainstem membranes with any of these anesthetics. The ability of guanine nucleotides to depress the high affinity binding of two agonists, carbamylcholine and [3H]oxotremorine-M, was decreased or eliminated after equilibration of brainstem membranes with any of the anesthetics. In each of these actions, these anesthetics resemble halothane and diethyl ether. These results indicate that interference with muscarinic receptor-G protein interactions is a common property of liquid volatile anesthetics and may represent a general mechanism for the disruption of signal transmission between cells during anesthesia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2501717&dopt=Abstract
Behav Neural Biol. 1987 Sep;48(2):206-12.
Effects of the nicotinic receptor blocker mecamylamine on radial-arm maze performance in rats.
Levin ED, Castonguay M, Ellison GD.
Department of Psychology, University of California, Los Angeles 90024.
Lesions of cholinergic neurons have been found by many investigators to impair choice accuracy in the radial arm maze. Because muscarinic receptor blockers, such as scopolamine, have also repeatedly been found to impair choice accuracy in the radial-arm maze, it has generally been thought that the critical effect of cholinergic lesions is the deafferentation of muscarinic receptors. The possible involvement of nicotinic receptors in the cholinergic bases of cognitive performance in the radial-arm maze has not been as well investigated. The present study examined the effects of the blockade of nicotinic receptors on performance of female Sprague-Dawley rats in the radial-arm maze. Acute administration of the the nicotinic receptor blocker, mecamylamine (10 mg/kg) was found to significantly impair radial-arm maze choice accuracy. This dose also caused a significant increase in response latency in the maze. The effect on choice behavior but not locomotor speed seemed to be due to the central effects of mecamylamine, because administration of the peripheral nicotine receptor blocker, hexamethonium (20 mg/kg), did not impair choice accuracy, even though it did increase response latency to a similar degree as the 10-mg/kg dose of mecamylamine. Lower doses of mecamylamine (2.5 and 5 mg/kg) did not impair choice accuracy. These results indicate that central nicotinic as well as muscarinic cholinergic receptors are involved with cognitive functioning.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2823791&dopt=Abstract
J Pharmacol Exp Ther. 1987 Jul;242(1):238-44.
Muscarinic acetylcholine receptor-mediated phosphoinositide turnover in cultured cerebellar granule cells: desensitization by receptor agonists.
Xu J, Chuang DM.
Cultured granule cells prepared from 8-day postnatal rats were used for the study of carbachol-induced phosphoinositide turnover. The addition of carbachol induced a 20- to 30-fold increase in [3H]inositol monophosphate (IP1) accumulation within 30 min in the presence of 20 mM LiCl in granule cells prelabeled with [3H]myoinositol. Carbachol also stimulated the formation of [3H]inositol bisphosphate and [3H]inositol trisphosphate assayed either in the presence or in the absence of lithium; the increase in [3H]inositol triphosphate and [3H]inositol biphosphate synthesis appeared to be faster in the time course but much smaller in amount when compared with the formation of [3H]IP1. The EC50 of carbachol was approximately 7 microM, and the saturation concentration was about 100 microM. This carbachol-induced response was completely blocked by two muscarinic acetylcholine receptor (mAChR) antagonists, atropine and pirenzepine, with a Ki of 0.5 and 120 nM, respectively. Saturation studies of the binding of [3H]N-methylscopolamine and [3H]quinuclidinyl benzilate to mAChRs in intact granule cells revealed the presence of a single class of binding sites with a Kd of 140 and 126 pM, respectively, and a Bmax of approximately 70 fmol/10(6) cells for both ligands. Within 1 hr after pre-exposure of cells to carbachol, the subsequent carbachol-induced [3H]IP1 accumulation was reduced by about 50%, whereas mAChR binding, assessed by using either [3H]N-methylscopolamine or [3H]quinuclidinyl benzilate, was unchanged. A second slower phase of desensitization was associated with a loss of mAChR binding sites; at 18 hr, the decrease of responsiveness was about 80%, whereas the loss of mAChR sites was about 60%.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3039110&dopt=Abstract
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