In glutamatergic transmission from crayfish motor nerve terminals, activation of presynaptic inhibitory autoreceptors shortens the delays of quantal releases. Glutamate binds to membrane transporters, and activation of a transporter-associated chloride conductance mediates shortening of release delays (Dudel 2005,Pflügers Arch. 449, Suppl. 1, O 02-2).In mammals neuromuscular transmission is cholinergic, and the presynaptic inhibitory receptors are of the muscarinic M2 type. It seemed of interest whether in this synaptic system, that is so different from the crayfish one, synaptic delays are also shortened by the agonist muscarine. In 10 experiments on diaphragms of 20 days old balb C mice at 20°C all solutions contained pirenzepine which blocks M1 receptors. Quantal releases were evoked by depolarising pulses through the recording electrode. Control solution or such containing 20 mM muscarine were superfused to a terminal through the recording macro-patch electrode. Relative to the controls muscarine shortended release delays highly significantly, by 42% during the first 0.5 ms of releases and by 11% during the first 1 ms. Using Kolgomoroff-Smirnov statistics, in 6 single experiments the shortening was highly significant with a < 0.001, in 2 with a < 0.05, and less significant in 2. It appears that shortening of synaptic delays during presynaptic autoinhibition could be a characteristic of synaptic transmission.