Resting non-quantal acetylcholine (ACh) and probably glutamate (Glu) release from nerve endings activates M1- and NMDA-receptor mediated Ca2+ entry into the sarcoplasm with following activation of NOS and production of NO. This is a trophic message from motoneurones which keeps the Cl– transport inactive in the innervated sarcolemma. After denervation, the secretion of ACh and Glu at the neuromuscular junction is eliminated within 3–4 h and the production of NO in the sarcoplasm is lowered. As a result, the Cl– influx is probably activated by dephosphorylation of the Cl– transporter with subsequent elevation of intracellular Cl– concentration. The equilibrium Cl– potential becomes more positive and the muscle membrane becomes depolarized.

        Key words: acetylcholine, carbachol, glutamate, atropine, nitric oxide, phosphorylation, denervation, chloride transporter, resting membrane potential