Drugs online research references
Receptors Channels. 1998;5(6):331-45.
Antagonist profile and molecular dynamic simulation of a Drosophila melanogaster muscarinic acetylcholine receptor.
Reaper CM, Fanelli F, Buckingham SD, Millar NS, Sattelle DB.
Babraham Institute Laboratory of Molecular Signalling, Department of Zoology, University of Cambridge, UK.
A stably-transfected, Drosophila cell line (S2-DMl-1) expressing the Drosophila DMl muscarinic acetylcholine receptor (mAChR) exhibits high-affinity, saturable, specific binding of the radiolabelled muscarinic antagonist [3H]-N-methyl scopolamine ([3H]-NMS) with an equilibrium dissociation constant (Kd) of 0.67 +/- 0.02 and a Bmax of 1.53 +/- 0.3 pmol/mg protein. Displacement of [3H]-NMS by mAChR antagonists results in the pharmacological profile: 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) > hexahydrosiladifenidol > p-fluorohexahydrosiladifenidol > nitrocaramiphen > pirenzepine > methoctramine > AFDX-116. This antagonist profile most closely resembles that of the vertebrate M3 mAChR subtype. In this study, however, we have demonstrated that the antagonist profile of DM1 is distinct from those of vertebrate mAChR subtypes. Molecular dynamic simulations of the Drosophila muscarinic receptor are presented in the free, carbamylcholine-bound and NMS-bound forms. Theoretical, quantitative structure-activity relationship models have been developed; a good correlation is observed between the interaction energies of the minimized ligand-receptor complexes and the pharmacological affinities of the antagonists tested.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9826910&dopt=Abstract
Regul Pept. 1993 Jun 11;45(3):353-62.
Galanin stimulates striatal acetylcholine release via a mechanism unrelated to cholinergic receptor stimulation.
Pramanik A, Ogren SO.
Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden.
The effect of galanin (GAL) on the basal and the muscarinic agonist/antagonist mediated release of acetylcholine (ACh) in the striatum was investigated in male rats using in vivo microdialysis and HPLC techniques. GAL (300 microM or 3 nmol/10 microliters), perfused through the microdialysis membrane into the striatum, was found to enhance basal ACh release. The GAL evoked ACh release was completely prevented by bupivacaine, a sodium channel blocker (1.5 mM) when coperfused with GAL. This suggests that the effect of GAL depends on intact neuronal activity and thus derives from impulse-dependent release. The muscarinic agonists oxotremorine (0.3 mg/kg, i.p.) or carbachol (100 microM, infusion) reduced ACh release and reduced the stimulation of ACh release by GAL with a magnitude corresponding to that of oxotremorine or carbachol alone. Thus, the resultant effect of GAL on ACh release remained unchanged. When GAL was given at a threshold dose (30 microM), which by itself did not stimulate ACh release, it was unable to attenuate the muscarinic agonist induced inhibition of ACh releases. Furthermore, GAL given in combination with scopolamine (0.25 mg/kg, i.p.) or pirenzepine (1 microM, infusion) added to the stimulating effect by the two muscarinic antagonists. In contrast to the GAL (300 microM) evoked ACh release, the scopolamine (0.25 mg/kg, i.p.) stimulated ACh release was not blocked by M15, a putative GAL antagonist, indicating that the mechanisms behind GAL and scopolamine evoked striatal ACh release differ. These results suggest that the mechanisms behind GAL evoked release do not involve direct interactions with pre- or postsynaptic muscarinic receptor mediated events. It is concluded that the stimulation of the basal ACh release by GAL in the striatum occurs via occupation of GAL receptors located on cholinergic interneurons and that the release process is dependent on intact neuronal activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7688904&dopt=Abstract
Eur J Pharmacol. 1998 Oct 23;359(2-3):211-21.
Muscarinic receptor subtypes in the porcine lung during postnatal development.
Hislop AA, Mak JC, Reader JA, Barnes PJ, Haworth SG.
Vascular Biology and Pharmacology Unit, Institute of Child Health, London, UK.
The responsiveness of the pulmonary circulation to acetylcholine changes in the newborn piglet. Therefore muscarinic receptors have been studied in the developing porcine lung from birth to adulthood using ligand binding, Northern blotting and in situ hybridisation. Maximal binding capacity of [N-methyl-3H] scopolamine and the affinity of the receptor in lung membranes increased between birth and 16 days (p < 0.05). Subtype affinity changed with age, but always M3, > M1 > M2. Northern blots of porcine muscarinic receptor subtypes showed m1, m2 and m3 mRNA present in lung membranes. m2 mRNA was present at all ages and decreased with age. m1 mRNA was absent at birth and m3 mRNA was absent at 3 days. Autoradiographic localisation showed ligand binding to the parenchyma and airway smooth muscle and nerves, there was no binding to intrapulmonary vessels. In situ hybridisation localised mRNA of all three subtypes to the smooth muscle cells of both vessels and airways. Changes in the receptor subtypes may explain the pharmacological changes during postnatal adaptation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9832393&dopt=Abstract
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