THE CONTRIBUTION OF NMDA AND NON-NMDA RECEPTORS TO FAST AND SLOW TRANSMISSION OF SENSORY INFORMATION IN THE RAT SL BARREL CORTEX

The main objective of this study was to establish the contribution of NMDA receptors to natural processing of somatosensory information with in rat SI barrel cortex. Responses of 52 cells in layers I-IV of the r at barrel cortex were analyzed by PSTH (peristimulus histogram) analys is of evoked spikes in reply to brief deflections of the principal whi sker in animals anesthetized with urethane. Short and longer peak late ncy responses within PSTHs were compared in the presence and absence o f the specific NMDA and non-NMDA antagoniStS D(-)-2-amino-5-phosphonov aleric acid and 6,7-dinitroquinoxaline-2,3-dione, which were administe red locally to neurons by iontophoresis and additionally tested agains t their putative specific agonists, NMDA and quisqualate, respectively . The results suggest the following. (1) The generation of most spikes from cells in layers I-IV is dependent upon activation of NMDA recept ors. However, NMDA receptors do not contribute to responses at very sh ort latencies commensurate with monosynaptic thalamocortical relay for layer IV cells. These appear to be entirely mediated through non-NMDA receptors. (2) In the absence of transmission through NMDA receptors, non-NMDA receptors do not generate significant spike activity in late r (10-100 msec latency) discharges. (3) NMDA receptor participation in first spike generation is directly dependent upon the latency of resp onse of the cell to principal whisker deflection. (4) Latency of respo nse, non-NMDA receptor-mediated spike generation and laminar location were powerfully covariant. (5) In addition, it was found that cells ex hibiting short-duration spikes (<0.7 msec; ''fast-spike units'') in la yer IV responded powerfully at short latencies, first spikes being ent irely dependent upon non-NMDA but not NMDA receptor action, later spik es (10-100 msec poststimulus) being >80% dependent upon NMDA receptor action. It is concluded that most sensorially driven spike activity in layers I-IV is dependent upon NMDA receptor action. This appears to b e enabled by contingent subthreshold depolarization largely through no n-NMDA receptor action, whereas the earliest thalamocortical discharge s are evoked solely through non-NMDA receptors.