Effects of low ozone-oxygen concentrations on the acetylcholine release at the mouse neuromuscular junction.

The use of a mixture of low concentrations of ozone (O3) with oxygen (O2) have been proved to be useful in different human pathological conditions. Owing to a lack of both pharmacological and epidemiological basic studies, the scientific consideration of this therapeutic potential is still inappropriate. Here, we started, from an electrophysiological point of view, a study on the possible effects of low O3 doses on the acetylcholine (ACh) release at the neuromuscular junction. Indeed, some experimental conditions indicate a positive effect either in maintaining cytosolic calcium (Ca2+) homeostasis or in increasing the efficacy of the intracellular antioxidant systems. Furthermore, a positive action on the kinetics of some antioxidant enzymes must be taken into account as a possible molecular mechanism in the regulation of the function of cellular homeostasis. Our data demonstrate a reduction of evoked ACh release in the mouse neuromuscular junction. O3 affects neither the spontaneous ACh release nor the kinetics of the ACh-receptor-channel complex. The results are compatible with a reduction of intracellular Ca2+ and proved a molecular action of O3.

Effects of glycine on the mouse neuromuscular junction.

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.