Drugs online research references
J Neurochem. 1999 Jan;72(1):58-65.
Cloning and expression of a G protein-linked acetylcholine receptor from Caenorhabditis elegans.
Lee YS, Park YS, Chang DJ, Hwang JM, Min CK, Kaang BK, Cho NJ.
Institute for Molecular Biology and Genetics, Department of Biology, Seoul National University, Korea.
We have isolated a cDNA clone from the nematode Caenorhabditis elegans that encodes a protein of greatest sequence similarity to muscarinic acetylcholine receptors. This gene codes for a polypeptide of 682 amino acids containing seven putative transmembrane domains. The amino acid identities, excluding a highly variable middle portion of the third intracellular loop, to the human m1-m5 receptors are 28-34%. When this cloned receptor was coexpressed with a G protein-gated inwardly rectifying K+ channel (GIRK1) in Xenopus oocyte, acetylcholine was able to elicit the GIRK current. This acetylcholine-induced current was substantially inhibited by the muscarinic antagonist atropine in a reversible manner. However, another muscarinic agonist oxotremorine and antagonists scopolamine and pirenzepine had little or negligible effects on this receptor. Taken together, these results suggest that the cloned gene encodes a G protein-linked acetylcholine receptor that is most similar to but pharmacologically distinct from muscarinic acetylcholine receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9886054&dopt=Abstract
Neuropharmacology. 1998 Dec;37(12):1503-13.
Effect of ventral tegmental 6-hydroxydopamine lesions on the locomotor stimulant action of nicotine in rats.
Louis M, Clarke PB.
Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Convergent evidence suggests that the locomotor stimulant effect of nicotine is mediated by nicotinic receptors located on mesolimbic dopaminergic neurons. However, 6-hydroxydopamine lesions of the ventral tegmental area, resulting in substantial depletion of nucleus accumbens dopamine, were recently reported to have no effect on nicotine-induced locomotion. The present study sought to re-examine this issue. Rats received bilateral infusions of 6-hydroxydopamine or vehicle into the ventral tegmental area. Starting 3 weeks later, locomotor activity was tested after subcutaneous injection of saline, nicotine (0.4 mg/kg base), amphetamine (0.5 mg/kg) or scopolamine (0.5 mg/kg). In lesioned animals, the locomotor stimulant effects of nicotine and amphetamine were greatly reduced, whereas saline and scopolamine-induced activity was scarcely affected. Dopamine denervation was assessed by autoradiography, using [125I]RTI-55 to label plasmalemmal dopamine transporters. Labelling was reduced in nucleus accumbens core and shell and in the ventral tegmental area (by 87, 81 and 70%, respectively), and in nigrostriatal areas (52-77%). The locomotor stimulant effects of nicotine and amphetamine were correlated with residual [125I]RTI-55 labelling in mesolimbic and nigrostriatal regions (r=0.6-0.8). The present results provide further evidence that the locomotor stimulant effect of nicotine is dependent on the integrity of ascending dopamine neurons.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9886673&dopt=Abstract
cric.chemres.hu
Specific binding of [3H]strychnine was studied on membranes prepared from rat spinal cord. Several antagonists and agonists of 5-HT3 receptors and tropane derivatives displaced [3H]strychnine binding with micromolar potencies. In the presence of 10 microM glycine a high affinity (nanomolar) component of displacement was also observed for the tropeines zatosetron, bemesetron and tropisetron. The displacing potency of glycine was also enhanced by these agents which are therefore termed glycine-positive. In contrast, atropine, SR 57227A, m-chlorophenylbiguanide, metoclopramide and granisetron are termed glycine-negative, because they decreased the displacing potency of glycine while glycine decreased the displacing potencies of atropine and metoclopramide. The dissociation of [3H]strychnine binding was accelerated in the presence of m-chlorophenylbiguanide, SR 57227A, atropine and zatosetron with a concentration dependence (EC50 values and Hill slopes) similar to their displacing effects. This demonstrates that the displacement of strychnine binding is associated with allosteric interactions between different binding sites. Structure-activity analysis revealed that the tropeine structure is essential for high affinity binding, and its substitutions (in scopolamine and cocaine) or its replacement (in ondansetron and metoclopramide) strongly decrease the potency and/or efficacy of allosteric modulation. High affinity modulatory sites for tropeines appear to be associated with the potentiation of ionophore function, but distinct from the low affinity channel blocking sites as well as from the binding sites of strychnine and glycine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9886686&dopt=Abstract
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