Interneurons involved in mediation and modulation of gill-withdrawal reflex in Aplysia. II. Identified neurons produce heterosynaptic facilitation contributing to behavioral sensitization.

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Abstract
Sensory motor and interneurons that participate in mediation of the gill-withdrawal reflex of Aplysia were identified previously. Neurons (L22, L28 and L29) that produce heterosynaptic facilitation that probably contribute to modulation of that reflex during behavioral sensitization were identified, as was a neuron (L16) that produced heterosynaptic inhibition of the same postsynaptic potentials (PSP). In the isolated abdominal ganglion, intracellular stimulation of a single L29 neuron produced facilitation of the complex PSP elicited in a gill or siphon motor neuron by stimulation of the siphon or branchial nerves in 27% of the cases. On average, the amplitude of the complex PSP increased by 119% compared to controls and remained at that level for up to 5 min following L29 stimulation. Stimulation of at least 2 different L29 cells in the same ganglion produced facilitation of the complex PSP. Stimulation of L22 and L28 neurons produced facilitation in 24 and 30% of the cases, respectively. Since all of these neurons normally fire during stimulation of a pleuroabdominal connective their combined action may be sufficient to account for the facilitation produced by connective stimulation, which is generally greater than that produced by stimulation of a single neuron. Stimulation of an L29 neuron produces facilitation of unitary sensory-to-motor neuron PSP which may be sufficient to account for most of the facilitation of the complex PSP by L29. Stimulation of L22 produced facilitation of the complex PSP by an additional mechanism: PTP [post-tetanic potentiation] at the interneuron-to-motor neuron synapse. Stimulation of L16 produced inhibition of the complex PSP, which outlasted the stimulation by about 1 min. The mechanism of this effect has not yet been investigated.