Local Circuit Connections Mediated by NMDA and Non-NMDA Receptors in Slices of Neocortex

Abstract

The extent to which NMDA receptors contribute to simple information transfer has been much debated and may vary from region to region. For example, a significant proportion of sensory input to the thalamus, particularly that mediating noxious input (Eaton & Salt, 1989), is blocked by NMDA antagonists while thalamocortical inputs are sensitive to non-NMDA EAA antagonists, not to NMDA antagonists (P.L. Herrling & T.E. Salt, personal communication). Despite the high density of NMDA binding sites in cortical regions, such as neocortex and hippocampus (Greenamyre et al, 1985), only a relatively small proportion of epsps (excitatory postsynaptic potentials) are demonstrably mediated by these receptors. Indeed, in the CA1 region of hippocampus, the component of the input from CA3 that is purported to be NMDA receptor mediated was only revealed when non-NMDA EAA receptors were blocked and the input pathway stimulated at high strength (Kauer, this volume, Andreasen et al, 1988). Since evidence first began to accumulate that several types of synaptic plasticity are blocked by NMDA antagonists (Collingridge et al, 1983, Artola & Singer, 1987, Kleinschmidt et al, 1987), NMDA receptors have come to be regarded as mediators of plasticity, rather than as mediators of rapid information transfer. Whether or not this distinction is absolute, any discussion of the function of NMDA receptor mediated synapses should include their probable role as mediators of synaptic plasticity.