Modulation of cholinergic transmission in the neuronal network of the gill and siphon withdrawal reflex in Aplysia.

Inhibitory interneurons are important elements of the network underlying the gill and siphon withdrawal reflex in Aplysia, and a large component of this inhibition is cholinergic. In this study, we investigated one key identified cholinergic inhibitory interneuron of the network, neuron L16, and studied some properties of its synaptic transmission and its modulation. We found that a slow inhibitory postsynaptic potential evoked in sensory neurons by L16 has two components. An earlier inhibitory postsynaptic potential component is sensitive to curare (100 microM) and has a reversal potential near the Cl- equilibrium potential (-54.5 mV). A later inhibitory postsynaptic potential component is sensitive to tetraethylammonium (0.5-1 mM); it is decreased by membrane hyperpolarization and becomes undetectable near the K+ equilibrium potential (between -80 and -90 mV). Input to sensory neurons from L16 can be altered by two neuromodulators of the reflex, the small cardioactive peptide and serotonin. Small cardioactive peptide (10 microM) facilitates the connections between L16 and the sensory neurons, while serotonin (5-10 microM) inhibits them. Part of the effect of serotonin on the transmission between L16 and the sensory neurons is due to a postsynaptic mechanism, since responses to acetylcholine application in these cells are decreased by serotonin. These results indicate an additional site of synaptic plasticity in the withdrawal reflex network, the inhibitory cholinergic transmission, by two major neuromodulatory transmitters, small cardioactive peptide and serotonin.