Abstract
Presynaptic facilitation of transmission from sensory to motor neurons contributes significantly to behavioral sensitization of defensive withdrawal reflexes in Aplysia. Presynaptic facilitation is associated with a decrease in the serotonin-sensitive K+ conductance. This decrease broadens the presynaptic action potential. In addition, the procedures that cause facilitation—stimulation of the connective (the pathway from the tail and head), application of modulatory transmitters, or injection of cAMP—also increase the excitability of the sensory neurons as tested with intracellular depolarizing pulses injected into the cell body. The increased excitability is reflected in a decreased threshold for generating action potentials and a reduction in accommodation to prolonged constant current stimuli. By influencing the excitability of the peripheral processes of the sensory neurons, stimulation of the connectives or serotonin also produces a small enhancement of the response of the sensory neurons to a tactile stimulus applied to the siphon. The excitability changes appear to result, at least in part, from the same cellular mechanisms that lead to broadening of the action potential, a cAMP-mediated closure of K+ channels. Therefore, these findings indicate that the same class of mechanisms can, in principle, have a dual action and provide further evidence for parallel processing in the modulation of transmitter release from a single neuron.
Keywords: K+ currents, second messengers, presynaptic facilitation, excitability, sensitization
Full text
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Selected References
These references are in PubMed. This may not be the complete list of references from this article.
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