Excitation of mammalian central neurones by acidic amino acids

Abstract

An investigation was made of the mechanism of depolarization of spinal motoneurones by excitant amino acids, and of possible antagonists of the excitation of spinal, thalamic and cerebral cortical neurones by these substances. The depolarization of motoneurones by dl-homocysteate was not altered by changes in intracellular chloride concentration, or extracellular concentrations of tetrodotoxin sufficient to suppress spike generation. The action of the amino acid thus probably resembles that of synaptically released excitatory transmitters. Of a number of substances tested only l-glutamic acid diethyl ester, l-methionine- dl-sulphoximine and 2-methoxy-aporphine reduced the sensitivity of spinal, ventrobasal thalamic, lateral geniculate and cerebral cortical neurones to l-glutamate, l-aspartate and dl-homocysteate without influencing excitation by acetylcholine. The spontaneous and synaptic firing of neurones were not markedly reduced by these antagonists. However, because of technical difficulties and the lack of selectivity of antagonism of excitation evoked by l-glutamate and l-aspartate, these antagonists were considered unsuitable for investigating synaptic excitatory pathways which may use either of these amino acids as transmitters.