Physostigmine blocked nicotinic acetylcholine receptors in rat sympathetic ganglion neurons
Abstract
AIM: 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.
CONCLUSION: 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.
Keywords:
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.
CONCLUSION: 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.