Additional component in the cellular mechanism of presynaptic facilitation contributes to behavioral dishabituation in Aplysia.

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Abstract
Sensitization of defensive gill and siphon withdrawal reflexes in Aplysia results, in part, from presynaptic facilitation of transmitter release from mechanoreceptor sensory neurons that innervate the siphon skin and synapse with interneurons and motor neurons. Presynaptic facilitation also can be elicited by application of serotonin. This facilitation is associated with two phenomena, a prolongation of the presynaptic action potential resulting from a decrease in a specific K+ current and an enhancement of the Ca2+ transients elicited by depolarization. Previous work has shown that prolongation of the action potential enhances synaptic transmission at normal levels of release. Here we report that an additional set of processes also contributes to facilitation. When repeated activation of the sensory neurons induces profound homosynaptic depression, prolonging the duration of action potentials (or of depolarizing commands under voltage clamp) has little effect on transmitter release. Nonetheless, serotonin is still capable of enhancing release. Since homosynaptic depression underlies the behavioral process of habituation, the second set of processes, by counteracting the consequences of the depression, seems to mediate the effects of dishabituation in the sensory neuron. Prolongation of the action potential by closure of the K+ channel seems to mediate the effects of sensitization.