Drugs online research references
Brain Res. 1993 Jul 16;617(1):28-36.
Activation of muscarinic receptors induces a long-lasting enhancement of Purkinje cell responses to glutamate.
Andre P, Pompeiano O, White SR.
Dipartimento di Fisiologia e Biochimica, Universita di Pisa, Italy.
The cerebellar cortex contains diffusely distributed cholinergic fibers and both muscarinic and nicotinic receptors. Behavioral studies suggest that an important function of this cholinergic innervation may be to modulate the effects of afferent input to the cerebellar cortex. The present study compared the effects of the muscarinic agonist bethanechol on basal firing rates and on glutamate-evoked firing of Purkinje cells in the vermis of the cerebellum of anesthetized rats. Microiontophoretic application of bethanechol produced a slowly developing, long-lasting enhancement of glutamate-evoked firing which was often disassociated from the bethanechol effect on the basal firing rate. Bethanechol increased the glutamate response of 22/33 Purkinje cells regardless of whether bethanechol increased, decreased or failed to alter the basal firing rate of the cell. The muscarinic antagonist scopolamine prevented the bethanechol-induced increase in the glutamate response. For 7/33 Purkinje cells, bethanechol decreased the glutamate-evoked response. However, this decrease did not appear to be mediated by muscarinic receptors because it was not blocked by scopolamine and it was mimicked by application of the vehicle alone. Acetylcholine application produced a long-lasting increase in the glutamate response of 4/5 Purkinje cells that was similar to the bethanechol effect. These data indicate that the cerebellar cholinergic system exerts a prominent modulatory influence on Purkinje cell excitability by acting through muscarinic receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8104084&dopt=Abstract
Farmaco. 1993 Jul;48(7):907-18.
Synthesis and muscarinic receptor binding profiles of antagonist benzotriazole derivatives.
Cappello B, Greco G, Novellino E, Perissutti E, Santagada V, Silipo C, Vittoria A, Di Carlo R, Meli R, Muccioli G.
Dipartimento di Chimica Farmaceutica e Tossicologica dell'Universita di Napoli, Italy.
A series of benzotriazole derivatives were synthesized and tested in order to determine their activities for muscarinic receptor subtypes (M1, M2 and M3). Binding affinities were measured as KI values by competition against [3H]-N-methylscopolamine in rat cortex, atria and ileum. Pharmacological in vitro tests were performed on isolated tissue preparations (rabbit vas deferens, guinea pig atria and ileum); the compounds showed antimuscarinic activity. The synthesized ligands were characterized by moderate activity; however, some of them displayed interesting selectivity profiles (M2/M1 and M2/M3); particularly, the selectivity exhibited by the benzotriazole derivative 14b was quite similar to that observed for AF-DX 116, a typical M2 specific antagonist.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8397675&dopt=Abstract
Nippon Shokakibyo Gakkai Zasshi. 1991 Aug;88(8):1571-8.
[Analysis of muscarinic receptors on rat pancreatic acini by using 125I-quinuclidinyl benzilate and N-[3H]-methylscopolamine]
[Article in Japanese]
Aoki E, Adachi H, Noguchi M, Satoh S, Ohnishi S, Honda T, Konishi J.
Department of Nuclear Medicine, Kyoto University School of Medicine.
To analyze muscarinic receptors on rat pancreatic acini, we studied the binding of 125I-quinuclidinyl benzilate (125I-QNB) and N-[3H]-methylscopolamine ([3H]-NMS) to these acini. Binding of 125I-QNB and [3H]-NMS to acini was specific and reversible. 125I-QNB bound to low affinity site, which was not recognised by [3H]-NMS. However, nonspecific binding of 125I-QNB to acini was very high (46%), so 125I-QNB may be inadequate to analyze muscarinic receptor on pancreatic acini. Muscarinic receptors are classified in two groups, M1 and M2, according to affinity of pirenzepine which binds to M1 receptor selectively. Pirenzepine was 530 times less potent than atropine in inhibiting the binding of 125I-QNB, and 250 times less potent than atropine in inhibiting the binding of [3H]-NMS. These results suggest that muscarinic receptors on pancreatic acini are mainly M2 receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1942611&dopt=Abstract
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