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 membrane of CA1 pyramidal cells in the rat during synaptic activation of N-methyl-D-aspartate (NMDA) receptors. Repetitive activation (3-5 Hz) of Schaffer collaterals provoked a NMDA receptor-mediated component in the field excitatory postsynaptic potential (fEPSP) within 15 s. The generation of this component follows a characteristic self-limiting cycle, vanishing after 6-10 s. When alvear shocks were paired to the orthodromic volleys, the antidromic population spike (PS) was completely abolished only if the NMDA receptor-mediated fEPSP had occurred. This blockade of antidromic invasion lasted for 120-150 ms after each orthodromic shock. A reduction in the safety factor for axon-soma transmission is presumed during NMDA receptor synaptic activation.