The effects of cholinergic drugs on the quantal contents of the nerve-evoked endplate currents (EPC) and the parameters of the time course of quanta release (minimal synaptic latency, main modal value of latency histogram and variability of synaptic latencies) were studied at proximal, central and distal regions of the frog neuromuscular synapse. Acetylcholine (ACh, 5x10-4M), carbacholine (CCh, 1x10-5M) or nicotine (5x10-6M) increased the numbers of EPCs with long release latencies mainly in the distal region of endplate (90-120 µm from the last node of Ranvier), where the synchronization of transmitter release was the most pronounced. The parameters of focally recorded motor nerve action potentials were not changed by either ACh or CCh. The effects of CCh and nicotine on quantal dispersion were reduced substantially by 5x10-7M (+)tubocurarine (TC). The muscarinic agonists, oxotremorine and propargyl ester of arecaidine, as well as antagonists, such as pirenzepine, AF-DX 116 and methoctramine, alone or in combination did not affect the dispersion of the release. Muscarinic antagonists did not block the dispersion action of CCh. Cholinergic drugs either decreased the quantum content mo (muscarinic agonist, oxotremorine M, and nicotinic antagonist, TC), or decreased mo and dispersed the release (ACh, CCh and nicotine). The effects on mo was related neither to the endplate region nor to the initial level of release dispersion. It follows that the mechanisms regulating the amount and the time course of transmitter release are different and that, among other factors, they are controlled by presynaptic nicotinic receptors.