For years, long-lasting plasticity of synaptic transmission was the favourite mechanism to account for information storage in the brain. While bidirectional long-term synaptic plasticity is computationally appealing (in part because of synapse-specific changes among a large array of inputs), it is not the whole story. Recent evidence indicates that the neuronal message is also persistently filtered through regulation of voltage-gated ion channels. Excitatory postsynaptic potentials (EPSPs) measured at the axon hillock result from a tight interplay between synaptic and intrinsic voltage-gated conductances that either amplify or attenuate the synaptic potentials (review in Spruston, 2008). Any modifications in this fragile equilibrium may in turn facilitate or diminish the probability that a given synaptic input triggers an action potential. For instance, induction of long-term synaptic potentiation (LTP) in CA1 hippocampal neurons down-regulates A-type K~+ (Frick et al. 2004) and hyperpolarization-activated cationic (H) currents (Campanac et al. 2008) in the dendrites, and in turn facilitates the generation of an action potential by the EPSP. In paired recordings of connected neurons, LTP is associated with an increase in excitability of the presynaptic neuron that results from a facilitation of the trans-
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