Effectors Of Pka And Pkc In Aplysia Presynaptic Facilitation

In attempting to understand how presynaptic facilitation in Aplysia sensory neurons occurs, it is worth considering the mechanisms normally operating to produce baseline neurotransmitter release (see figure). First, stimulation of siphon sensory neuron nerve endings in the gill and siphon complex (e.g., by light touch) leads to membrane depolarization and generation of an action potential. Invasion of the action potential into the presynaptic terminal causes the opening of voltage-gated calcium channels, which are open for a period of time proportional to the duration of the action potential. Of course, the invasion of multiple action potentials will also elicit additional calcium influx. This calcium signal triggers activation of the molecular machinery leading to fusion of neurotransmitter-containing vesicles with the sensory neuron presy-naptic membrane, resulting in release of neurotransmitter into the synaptic cleft.

By and large, presynaptic facilitation is achieved by modulation of three sites in the cascade of events resulting in neurotransmitter release. One site is closure of "S"-channels, or serotonin-sensitive potassium channels. A second site is modulation of Ikv, or voltage-sensitive potassium channels. Finally, there is modulation of the responsiveness of the neurotransmitter release machinery to the action potential-associated calcium influx. In the remainder of the section, I will briefly describe the impact of the alterations of each of these sites.

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