Organophosphorus nerve agent mechanism

Pyridostigmine bromide competitively binds to nerve tissue AchE. The binding is reversible and has been shown to protect AchE against irreversible inhibition by organophosphorus nerve agents. Pyridostigmine is a quarternary compound and does not readily cross the blood-brain barrier. Thus, it is not expected to affect or protect brain AchE. Cholinesterase inhibition, which is a mechanism of action, is also responsible for toxicity. 

Of the various mechanisms of action ascribed to nerve CW agents in various in vitro model systems, most appear to be active at concentrations where significant inhibition of AChE would be expected to occur. These conditions are unlikely to be seen in the absence of recognizable cholinergic toxicity and hence would not be classified as a low-dose effect. The one effect that seems to occur at a sufficiently low concentration of organophosphorus anticholinesterase to be considered a low-dose phenomenon is the slow allosteric modulation of muscarinic receptors regulating presynaptic release of other neurotransmitters. The observation that this allosteric modulation requires several hours to develop suggests that this mechanism would most likely be applicable to a subacute or subchronic exposure rather than one seen after a brief, acute dose. 

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