Drugs online research references
Eur J Pharmacol. 1993 Jan 19;230(3):313-20.
Development of tolerance to amnesic effects of chlordiazepoxide in relation to GABAergic and cholinergic neuronal systems.
Ishihara S, Hiramatsu M, Kameyama T, Nabeshima T.
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Meijo University Nagoya, Japan.
Chronic administration of benzodiazepines has been reported to produce tolerance in animals and humans. We investigated whether benzodiazepines produce tolerance to the amnesic effects and effects on benzodiazepine receptors, GABAergic and/or cholinergic neuronal systems of repeated administration of chlordiazepoxide, using a passive avoidance task and autoradiographic techniques. Tolerance developed to the amnesic effect of chlordiazepoxide when the drug was administered at a dose of 30 mg/kg (i.p.) once a day for 14 days. Bicuculline (1.0 and 1.5 mg/kg), a GABAA receptor antagonist, did not induce amnesia in normal mice, but did so in chlordiazepoxide-tolerant mice. Muscimol (0.25 mg/kg), a GABAA receptor agonist, in combination with a low dose of chlordiazepoxide, induced amnesia in normal mice, but not in chlordiazepoxide-tolerant mice. Scopolamine, an acetylcholine receptor antagonist, induced amnesia in normal mice, but not in chlordiazepoxide-tolerant mice. In the autoradiographical study, although repeated treatment with chlordiazepoxide had no effect on [3H]flunitrazepam and [3H]Ro 15-4513 binding to benzodiazepine receptors, it decreased [3H]muscimol binding to GABAA receptors, with a decrease in affinity in the cortex and hippocampus. Furthermore, repeated administration of chlordiazepoxide increased [3H]quinuclidinyl benzilate binding to muscarinic acetylcholine receptors in the hippocampus. These results suggest that tolerance develops to the amnesic effects of chlordiazepoxide, and that tolerance may be due to down-regulation of GABAA receptors and/or up-regulation of acetylcholine receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8382617&dopt=Abstract
Clin Exp Hypertens. 1993 Mar;15(2):409-21.
Muscarinic receptors in the aortae of normo- and hypertensive rats: a binding study.
Sim MK, Manjeet S.
Department of Pharmacology, Faculty of Medicine, National University of Singapore.
The muscarinic receptors in the aorta of the normo- and hypertensive rats were characterised with tritiated acetylcholine (3H-ACh) and various muscarinic receptor antagonists. The binding of 3H-ACh to the endothelial membranes of the normotensive Wistar Kyoto rats (WKY) and the spontaneously hypertensive rats (SHR) was displaceable by nanomolar range of scopolamine but only by micromolar range of atropine and homatropine. The reverse was observed with the muscle binding sites, i.e. the 3H-ACh was displaceable by nanomolar range of atropine and homatropine but only by micromolar range of scopolamine. Pirenzepine and 4-diphenyl-acetoxy-N-methyl-piperidine metobromide (4-DAMP) displaced the binding of 3H-ACh from both tissues in the nano to micromolar range, with the displacement from the endothelial binding sites occurring at lower concentration range of the ligands. The apparent IC50 values of both compounds for the smooth muscle were 9 and 16 times greater than those for the endothelial binding sites respectively. When saturated with guanylyl-imididiphosphate (GppNHp), conversion of high to low-affinity binding site occurred in both tissues of the WKY but only in the smooth muscle of the SHR. GppNHp had no apparent effect on the binding of 3H-ACh to the endothelial binding sites confirming that the high-affinity site for 3H-ACh was missing in the endothelium of the SHR.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8467326&dopt=Abstract
Psychopharmacology (Berl). 1983;79(2-3):226-30.
Cholinergic manipulation of perioral behaviour induced by chronic neuroleptic administration to rats.
Rupniak NM, Jenner P, Marsden CD.
Rats treated continuously for 4 months with haloperidol (1.4-1.6 mg/kg/day), trifluoperazine (4.5-5.1 mg/kg/day), or sulpiride (102-110 mg/kg/day), but not clozapine (23-26 mg/kg/day), exhibited an increased frequency of chewing jaw movements. Chewing in both control and haloperidol-treated rats was increased by acute administration of the cholinergic agents pilocarpine or physostigmine. Physostigmine or pilocarpine also induced abnormal gaping jaw movements; physostigmine-induced gaping was more prevalent in haloperidol-treated rats than control rats receiving physostigmine alone. Acute administration of the anticholinergic agents scopolamine and atropine decreased chewing in control animals and reduced haloperidol-induced chewing to control values or below. The effects of these cholinergic manipulations suggest that neuroleptic-induced perioral responses in rats do not resemble tardive dyskinesia in man.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6133305&dopt=Abstract
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