Glycine was applied at a range of different concentrations to test possible effects at the neuromuscular junction of the mouse. The presynaptic control of acetylcholine (ACh) release and the postsynaptic activation of the nicotinic receptor have been analysed by means of extracellular recording with an EPC7 Patch Clamp amplifier. The results indicated that glycine did not modify in a significant manner the release of ACh and the postsynaptic cholinergic receptor function. Nevertheless, a significant increase in the rate of the conformational change of the receptor-ion channel complex seemed to be noteworthy. Glycine at 30 and 300 microM increased in a dose dependent manner the decay time of the spontaneous miniature current. Concentrations of glycine exceeding 10mM completely blocked the activity of the end-plate in this preparation. In conclusion, we proved that glycine does not affect most of the parameters of neurotransmission in the mouse but, it increases the conformational change of the postsynaptic complex, perhaps inhibiting the acetylcholinesterase activity.