Abstract
Presynaptic I h channels become activated during a tetanus through membrane hyperpolarization resulting from Na + accumulation and electrogenic Na +/K + exchange. I h activation is obligatory for inducing long-term facilitation (LTF), a long-lasting synaptic strengthening. cAMP-induced synaptic enhancement also requires I h activation, and both processes are sensitive to actin depolymerization. Other mechanisms are responsible for expression of the responses. Once initiated, continued response to cAMP is I h and actin independent. Moreover, LTF-induced activation of I h renders subsequent cAMP enhancement insensitive to both I h blockers and actin depolymerization. This actin-stabilized “temporal synaptic tagging” set by I h activation is prolonged when I h is activated concurrent with an elevation in presynaptic calcium concentration ([Ca 2+] i), permitting the further strengthening of synapses given appropriate additional stimuli.
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