ABSTRACT
Glutamic acid is the main excitatory neurotransmitter of the mammalian central nervous system (CNS) and mediates neurotransmission across most excitatory synapses (1). Soon after the earliest description of the marked excitatory action of L-glutamic acid on the general electrical activity of the mammalian cerebral cortex (2), it became evident that a variety of amino acids had a depolarizing effect on single neurons of the CNS (3), the most potent of which was the synthetic derivative of the D-form of the naturally occurring L-aspartic acid, N-methyl-D-aspartic acid (NMDA) (4). In the following decades, a huge number of electrophysiological and pharmacological studies, together with the development of selective antagonists, led to the unequivocal distinction of NMDA receptors, within the wide variety of glutamate receptors, as those selectively activated by NMDA (5).
