BLOCKADE OF ANTIDROMIC INVASION OF CA1 PYRAMIDAL CELLS DURING SYNAPTIC ACTIVATION OF NMDA RECEPTORS

We have studied in situ the excitability state of the axon-soma membra ne of CA1 pyramidal cells in the rat during synaptic activation of N-m ethyl-D-aspartate (NMDA) receptors. Repetitive activation (3-5 Hz) of Schaffer collaterals provoked a NMDA receptor-mediated component in th e field excitatory postsynaptic potential (fEPSP) within 15 s1. The ge neration of this component follows a characteristic self-limiting cycl e, vanishing after 6-10 s1. When alvear shocks were paired to the orth odromic volleys, the antidromic population spike (PS) was completely a bolished only if the NMDA receptor-mediated fEPSP had occurred. This b lockade of antidromic invasion lasted for 120-150 ms after each orthod romic shock. A reduction in the safety factor for axon-soma transmissi on is presumed during NMDA receptor synaptic activation.