Psychiatry related information on PROPYLBENZILYLCHOLINE MUSTARD

• Blockade of cholinergic receptors by an irreversible antagonist, propylbenzilylcholine mustard (PrBCM), in the rat cerebral cortex causes deficits in passive avoidance learning [1].

High impact information on PROPYLBENZILYLCHOLINE MUSTARD

• Third, IC50 values as determined by competition of PZ for PrBCM binding sites were shifted to lower concentrations in superficial layers by ATN lesions but not in deep layers where the thalamus does not terminate [2].
• Muscarinic receptors from human, dog, and rat brain, rat and dog cardiac muscle, and guinea pig ileum longitudinal smooth muscle labeled with [3H] propylbenzilylcholine mustard, a covalent affinity reagent, appeared as single polypeptides with molecular weights of 80,000 on NaDodSO4-polyacrylamide gels [3].
• In the cerebral cortex, in hippocampus, and in N1E-115 cells, PrBCM treatment resulted in a loss of the PPI response, as measured by the release of [3H]inositol phosphates, that was equal to or greater than the reduction in receptor number, as determined by the loss of either [3H]quinuclidinylbenzilate- or [3H]N-methylscopolamine-binding sites [4].
• To determine whether the presence of a muscarinic receptor (mAChR) reserve might account for these differences, we have examined the effect of propylbenzilylcholine mustard (PrBCM) on mAChR number and on agonist-stimulated PPI hydrolysis [4].
• Gallamine did not protect against receptor alkylation by propylbenzilylcholine mustard, and [3H]QNB dissociation was apparently slowed by gallamine [5].

Biological context of PROPYLBENZILYLCHOLINE MUSTARD

• Propylbenzilylcholine mustard increased cell number, but interfered with cell-plastic attachment and spreading [6].
• Alkylation of muscarinic receptors by propylbenzilylcholine mustard antagonized the actions of soman on both spontaneous and electrically-evoked muscle contractions [7].

Anatomical context of PROPYLBENZILYLCHOLINE MUSTARD

• To guide the formulation of the model itself and to define the various parameters, data were combined from assays performed under various conditions with native membranes and following irreversible blockade of about 80% of the receptors with propylbenzilylcholine mustard [8].
• In order further to elucidate the role of muscarinic receptors in ganglionic transmission their distribution in the rat superior cervical sympathetic ganglion was investigated autoradiographically by use of the tritiated irreversible muscarinic ligand propylbenzilylcholine mustard [9].
• Delivery of receptors to the plasma membrane was measured by irreversible alkylating receptors already at the cell surface with propylbenzilylcholine mustard (PrBCM) and then following the recovery of binding of the polar radioligand [3H]-N-methylscopolamine ([3H]-NMS) in intact cells [10].
• In unanaesthetized cats the effects were examined of propylbenzilylcholine mustard (PrBCM) on injection into the cannulated cerebral ventricles and cisterna magna [11].
• To test the hypothesis that the putative muscarinic receptor subtypes in rat forebrain are interconvertible states of the same receptor, the selective antagonist pirenzepine (PZ) was used to protect muscarinic receptors from blockade by the irreversible muscarinic receptor antagonist propylbenzilylcholine mustard (PBCM) [12].

Associations of PROPYLBENZILYLCHOLINE MUSTARD with other chemical compounds

• Distance between the propylbenzilylcholine mustard attachment site and carbohydrates and thiol groups in muscarinic acetylcholine receptor protein from rat cerebral cortex [13].
• After treatment with propylbenzilylcholine mustard, carbachol induced contraction only in the presence of extracellular Ca2+ [14].
• In the absence of PZ, treatment of cerebral cortical membranes with 20 nM PBCM at 4 degrees C for 50 min resulted in a 69% reduction in the density of M1 binding sites and a 55% reduction in the density of M2 binding sites with no change in the equilibrium dissociation constants of the radioligands [3H]quinuclidinyl benzilate or [3H]PZ [12].
• Guanosine 5'-triphosphate converts some populations of propylbenzilylcholine mustard-sensitive muscarinic cholinoceptor sites to sites resistant to the drug in intestinal smooth muscle [15].
• The electrophoretic studies of prelabeled immunoprecipitated proteins revealed a peak of [3H] propylbenzilylcholine mustard with an apparent molecular weight similar to that of mAchR, which disappeared in the presence of atropine [16].

Gene context of PROPYLBENZILYLCHOLINE MUSTARD

• PBCM did not appear to discriminate putative M1 and M2 binding sites but selectively alkylated the high affinity NMS and QNB binding sites [17].

Analytical, diagnostic and therapeutic context of PROPYLBENZILYLCHOLINE MUSTARD

• In order to determine whether a reserve population of either of these receptors is present in this cell culture, the irreversible muscarinic receptor antagonist, propylbenzilylcholine mustard (PBCM), was used at different concentrations to bind various proportions of available muscarinic receptors [18].
• The characteristics of the putative subtypes of muscarinic receptors and their stimulation of phospholipase C was examined after treatment with two alkylating agents, N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline and propylbenzilylcholine mustard [19].
• The association of ATN afferents with muscarinic receptors was also explored by means of in vitro receptor autoradiography with the muscarinic ligands propylbenzilylcholine mustard (PrBCM) and pirenzepine (PZ) in normal rats and rats with ablations [20].

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