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Computational Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037, USA.

1. Pairing low-frequency orthodromic stimulation with high-frequency antidromic conditioning of pyramidal cells in area CA1 of the rat hippocampus resulted in long-lasting potentiation of the extracellular population spike of the cells, without an accompanying increase in the extracellular excitatory postsynaptic potential (EPSP), indicating an increase in EPSP-spike (E-S) coupling, also called E-S potentiation. 2. The amplitude of the antidromically conditioned E-S potentiation took up to 60 min to reach its peak, much longer than synaptic long-term potentiation (LTP) induced by orthodromic tetanic stimulation. 3. The population spike amplitude of a control orthodromic input, which stimulated a separate set of fibres and which was inactive during the pairing, was also increased in over half the slices tested. That it can affect a silent pathway suggests that antidromically conditioned E-S potentiation is not generated locally at tetanized synapses. 4. Bath application of 50 microM D,L-2-amino-5-phosphonovaleric acid (AP5) blocked induction of antidromically conditioned E-S potentiation. After washing out the AP5, the same stimulation resulted in population spike increases. This suggests that activation of the NMDA subtype of glutamate receptor is necessary for the induction of this form of E-S potentiation. 5. Application of 10 microM picrotoxin and/or 10 microM bicuculline, which block inhibition mediated by gamma-aminobutyric acid A (GABAA) receptors, did not reduce antidromically conditioned E-S potentiation. Thus, plasticity in GABAA-mediated inhibition cannot account for the increased population spike amplitude. 6. E-S potentiation did not increase the amplitude of either extracellular or intracellular EPSPs recorded at the cell body.

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