Physostigmine blocked nicotinic acetylcholine receptors in rat sympathetic ganglion neurons.
OBJECTIVE
To study the blocking mechanism of physostigmine (Phy) on nicotinic acetylcholine receptors (NAChR) in sympathetic neurons.


METHODS
The whole-cell patch-clamp technique was used to observe the effects of Phy on NAChR in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG).


RESULTS
Phy 5 -20 mumol.L-1 inhibited neuronal NAChR in a concentration-dependent manner and accelerated the desensitization of NAChR. Changing the membrane potential from -50 to -90 mV did not affect the blocking effect of Phy. Phy 200 mumol.L-1 did not induce any noticeable response in SCG neurons.


CONCLUSIONS
Phy blocked NAChR in the sympathetic ganglion neurons by interacting with the allosteric sites out of the binding sites and the open ionic channels of the receptors. Phy did not possess excitative effect on NAChR in SCG neurons.
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D002800:Cholinesterase Inhibitors / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010830:Physostigmine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011978:Receptors, Nicotinic / Q000187:drug effects*; D017783:Superior Cervical Ganglion / Q000187:drug effects*