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In CA1 hippocampal pyramidal neurons, after induction of LTP, postsynaptic spike firing increases more than would be expected from synaptic LTP, a phenomenon referred to as EPSP-to-spike (E-S) potentiation ( Bliss and Lomo, 1973 Andersen et al., 1980). In contrast to the detailed analysis of synaptic long-term potentiation (LTP), a cellular model for learning and memory ( Bliss and Collingridge, 1993 Malenka and Nicoll, 1999 Choi et al., 2000), less attention has been given to activity-dependent changes in the intrinsic excitability of neurons.

The intrinsic excitability of neurons has a crucial impact on the function of neural networks and is modified during the learning task in a variety of species ( Alkon et al., 1985 Cleary et al., 1998 Antonov et al., 2001 Burrell et al., 2001 Aizenman et al., 2003). This new form of hippocampal neuronal plasticity could be a cellular correlate of learning and memory besides synaptic LTP. The results suggest that induction of LTP-IE shares a similar signaling pathway with the late phase of synaptic LTP and requires activation of the NMDA glutamate receptor subtype, Ca 2+ influx, activity of CaM kinase II, and function of the protein synthesis. Induction of LTP-IE was blocked by the NMDA receptor antagonist APV, intracellular BAPTA, the CaM kinase inhibitors KN-62 and autocamtide-2-related inhibitory peptide, and the protein synthesis inhibitors emetine and anisomycin. Cell-attached patch recording of VGSC activities indicated such an activity-dependent change in VGSCs. LTP-IE was manifested as a decrease in the action potential threshold that was attributable to a hyperpolarized shift in the activation curve of voltage-gated sodium channels (VGSCs) rather than activity-dependent changes in synaptic inputs or A-type K + channels. By stimulating hippocampal CA1 pyramidal neurons with synaptic inputs correlating with postsynaptic neuronal spikes, we elicited an LTP of intrinsic excitability (LTP-IE) concurring with synaptic LTP. In contrast to the detailed analysis of long-term potentiation (LTP), less attention has been given to activity-dependent changes in the intrinsic neuronal excitability. The efficiency of neural circuits is enhanced not only by increasing synaptic strength but also by increasing intrinsic excitability.

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