High-affinity activation by paraoxon of a muscarinic receptor subtype in rat brain striatum
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Cited by (68)
Protective effects of mecamylamine and atropine against α<inf>4</inf>β<inf>2</inf> nicotinic receptor expression and functional toxicity in paraoxon-treated rats
2008, Environmental Toxicology and PharmacologyCitation Excerpt :Finally, benzodiazepines, administered to control AChE inhibitor-related seizures (Holstege et al., 1997), are likely to depress brainstem respiratory and circulatory centers and may thus potentiate known depressant effects of OPs or carbamates on these centers (Munro et al., 1990). In addition to inhibition of AChE, several organophosphates bind to both muscarinic and nicotinic acetylcholine receptors acting as receptor agonists (Jett et al., 1991) or antagonists depending on the organophosphate, receptor and the cell type (Oortgiesen et al., 1996; Van den Beukel et al., 1996). It has been demonstrated that nicotinic acetylcholine receptors (nAChRs) identified in mammalian brain, form pentameric heteromeric or homomeric ion-channels that are composed of different (α2–α7, α9–α10, and β2–β4) transmembrane subunits (Millar, 2003).
Evaluation of nicotinic receptors agonists and antagonists against paraoxon exposed PC12 cells
2008, Environmental Toxicology and PharmacologyCitation Excerpt :In addition to inhibition of AChE, several OPs also interact directly with receptors of the cholinergic system or modulate the receptor expression levels (Slotkin, 2004a). Organophosphates bind to both muscarinic and nicotinic receptors acting as a receptor agonists (Jett et al., 1991) or antagonists depending on the organophosphate, receptor and the cell type (Oortgiesen et al., 1996; Van den Beukel et al., 1996). Modification of ACh by conversion of its ester group to a carbamate yields the hydrolysis-resistant analogue carbamylcholine (carbachol).
Function-specific blockage of M<inf>1</inf> and M<inf>3</inf> muscarinic acetylcholine receptors by VX and echothiophate
2006, Brain ResearchCitation Excerpt :Namely, competition studies with the muscarinic antagonists, [3H]quinuclidinyl benzilate ([3H]QNB) and [3H]pirenzepine ([3H]PZ), did not show any evidence of binding of soman, sarin and tabun to rat cortical membranes, VX and echothiophate displayed competitive binding with Ki values in the μM range (Bakry et al., 1988) and paraoxon demonstrated non-competitive binding with 20% displacement (Katz and Marquis, 1989). On the other hand, soman, sarin, tabun, VX, echothiophate, and paraoxon displaced the agonist—[3H]cis-dioxolane ([3H]CD) with Ki values of 1–800 nM (50–100% displacements) in brain (Bakry et al., 1988; Jett et al., 1991; Ward et al., 1993) and heart membranes (Silveira et al., 1990). These results do not seem to allow for speculation regarding the nature of the OP muscarinic binding site and obviously do not permit prediction of the effect of the OP binding on the putative biochemical events triggered by receptor occupancy.
Behavioral toxicity of cholinesterase inhibitors
2006, Toxicology of Organophosphate & Carbamate Compounds
- 1
Permanent address: U.S. Fish and Wildlife Service, Patuxent Wildlife Research Center, Laurel, MD 20708.
- 2
Permanent address: Alexandria University, Faculty of Agriculture, Department of Plant protection, Pesticide Chemistry Division, Faculty of Agriculture, Alexandria, Egypt.