A behavioral reflex mediated by identified motor neurons in the abdominal ganglion of Aplysia undergoes two simple forms of shortterm modification. When the gill-with-drawal reflex was repeatedly evoked by a tactile stimulus to the siphon or mantle shelf, the amplitude of the response showed marked decrement (habituation). After a period of rest the response showed spontaneous recovery. The amplitude of a habituated response was facilitated by the presentation of a strong tactile stimulus to another part of the animal (dishabituation). Many characteristics of habituation and dishabituation in Aplysia are similar to those in vertebrates.

We have examinived the nieural correlates of habittuatiotn atid dishabitiuation of tlhe gill-withdrwal reflex in Aplysia. We obtained intracelllular recordings from identified gill motor neurons in the abdominal ganglionz of a semi-intact preparation of Aplysia wlhile we simultaneously recorded behavior responises of the gill. Habituation and dishabituation were not due to peripheral changes in either the sensory receptors or the gill musculature butt were caused by changes in the amplitlude of the excitatory synaptic potentials produced at the gill motor neurons.

Sensitization of the gill withdrawal reflex in Aplysia californica is an elementary form of learning, in part resulting from presynaptic facilitation of the LE mechanoreceptor neurons of the abdominal ganglion. It has previously been established that either application of serotonin or direct stimulation of a group of facilitatory neurons, the L29 cells of the abdominal ganglion, can simulate the effect of physiological stimulation in producing presynaptic facilitation. Because the evidence that serotonin serves as a facilitatory transmitter was indirect, we examined the distribution of serotonin-immunoreactive fibers and cell bodies in the abdominal ganglion in order to answer two questions: (1) do the sensory neurons receive serotonergic innervation and (2) are the L29 cells serotonergic? We observed two distinctive patterns of serotonergic innervation within the ganglion, sparse and dense. The sparse pattern is correlated with a serotonin-stimulated increase in cAMP in identified target cells, while the dense innervation is not. We found a sparse distribution of serotonin-immunoreactive fibers with varicosities close to both cell bodies and processes of identified LE sensory cells. It therefore is likely that the sensory neurons do receive serotonergic innervation. We also mapped the population of serotonergic neuronal cell bodies in the ganglion, and found five clusters of neurons. Cells in one of these clusters, the identified RB neurons, had previously been shown to synthesize serotonin from tryptophan and to contain the neurotransmitter in high concentration. Identified L29 facilitator cells marked by injection with Lucifer Yellow do not contain serotonin immunoreactivity and therefore evidently are not a source of serotonergic input onto sensory cells.