ABSTRACT
Glutamate mediates transmission at most central excitatory synapses. The modulation of synaptic activity of those synapses is responsible for several forms of plasticity involved in learning and memory (Nakanishi, 1992). Excessive release of glutamate has been implicated in acute, as well as in slow, neuronal death associated with pathologies such as ischaemia, epilepsy, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s chorea and Alzheimer’s disease (Choi, 1988; Olney, 1991). Fifteen years ago, our conception of synaptic activation of glutamate receptors was simply explained by fast postsynaptic currents generated by AMPA receptor channels and a slower response generated by calcium-permeable NMDA receptor channels. Today, the glutamatergic synaptic transmission appears more complex.
