Forskolin counteracts the effects of the organophosphate soman at the neuromuscular junction.
When neuromuscular transmission had been blocked using an organophosphate, function could be restored by treatment of the muscle with forskolin which increases the rate of desensitization of the nicotinic acetylcholine receptor. This suggests that excess post-synaptic depolarization due to acetylcholinesterase inhibition might be reversed by procedures which promote receptor desensitization.
Neuropsychiatry Research Program, School of Medicine, University of Alabama, Birmingham 35294.
R J
RJ
Bradley
M T
MT
Edge
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D005576:Colforsin / Q000494:pharmacology*; D003964:Diaphragm / Q000294:innervation / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D051381:Rats; D012999:Soman / Q000494:pharmacology*
D005576:Colforsin; D012999:Soman