Patch clamp studies on `embryonic´ neuromuscular nicotinic receptors have shown that low CTX concentrations block only the αδ binding site, allowing binding of ACh at the αγ site that elicits short single channel openings and short bursts with < 1 ms duration. In muscles of < 5 days old mice, CTX reduced the amplitudes and the decay time constants of quantal EPSCs (qEPSCs) and increased their rise times (Stock et al. 2013). In adult muscle the γ- is replaced by the e-subunit, and we intended to compare the results on `embryonic´ muscles to effects of CTx on transmission in adult muscles. EPSCs were elicited by 1 ms depolarisation pulses and also recorded through a perfused macropatch electrode. Application of 20 nM CTx for 20 min reduced the amplitude of qEPSCs to a fourth and increased their rise times. The distribution of decay time constants of the qEPSCs contained 2 components: the control one and a shorter one that is generated by CTx-blocked qEPSCs. 2 nM CTx applied for 3 hours reduced amplitudes of qEPSCs with a constant average slope of 4.6 ^.10^-5/s to less than half that indicates an equilibrium concentration of the block below 1 nM. The slopes of blocks increased in proportion to CTx concentrations up to 100 nM, as expected for binding at one site only. The respective rate of block of the αδ binding site of the nicotinic receptor by CTx is 1.8 10⁴ s^-1M^-1 which is 20 times lower than the rate of competitive block by procaine. - ^.In addition to the postsynaptic effects, the low CTx concentrations severely reduced the rate of release of quanta by activating presynaptic M2 receptors. When this dominant inhibition was prevented by blocking the M2 receptors with methoctramine, CTx activated M1 receptors that facilitated release. - Although containing partly different subunits, the reactions of `embryonic´ and of adult nicotinic receptors to block by CTx are at least qualitatively the same.