ABSTRACT
The present work with consideration to the autoradiographic pictures, suggests that cholinergic receptors are located at the gate of a channel originating from synaptic cleft coming to lie within the muscle fibre. ACHE molecules stand at the gate of this channel;controlling the entrance of different cholinergic agents. It was reported previously that dtc molecules stabilize the ACHE molecules and will obstruct the gate. This blocks the acess of ionic flux within the channel thus producing a non-depolarizing neuromuscular paralysis.The presented experiments imply that depolarizing agent will bring a considerable change in conformation of ACHE molecule and this causes the opening of the gate allowing ionic flux and depolarization .In case of ACh this process is repeated in a fraction of milli second, due to rapid regeneration of AChE while in case of suxamethonium and neostigmine [given in high dose], the regeneration of AChE takes much longer time thus will produce a depolarizing blockade. In this hypothesis the main responsability of AChE is confined to identification of cholinergic agents and cooperation in their function so, it can be accepted as cholinergic receptor. In regard to clinic, this work suggests that only the use of minimum effective dose of neostigmine is advisable fin reversing curarisation. In contrast to general belief the dose of neostigmine should be selected in relation to receptor dtc occupation and not depending on patient's weight. As it was demonstrated the early use of high dose of neostigmine may also potentiate curarisation