IT was recently proposed1 that the action of strychnine at spinal inhibitory synapses may be explained by an antagonism between strychnine and acetylcholine, an interaction between acetylcholine and presynaptically located receptors which are sensitive to strychnine being an essential requirement for the release of the inhibitory transmitter. This proposal, which would “eliminate blockade by strychnine as an essential qualification for the identification of a putative inhibitory transmitter” in the mammalian spinal cord, is based on the finding that strychnine, in concentrations of the order of 3–300 × 10−6 molar, reduces the release of acetylcholine by impulses in the preganglionic terminals of the perfused feline superior cervical ganglion.