Abstract
We have explored the morphological basis of the synaptic depression that underlies short-term habituation of the gill-withdrawal reflex in Aplysia by examining the fine structure of the presynaptic terminals of identified sensory neurons--a critical site of plasticity for the biochemical and biophysical changes that underlie this elementary form of learning. The structure of sensory neuron synapses from control (unstimulated) cells was compared with that of sensory neuron synapses from cells in which synaptic transmission had been depressed by repeated activation. We focused our analysis, as we had in an earlier study of long-term memory (Bailey and Chen, 1983), on the morphology of active zones at sensory neuron synapses. We found that both the incidence and size of serially reconstructed active zones were not changed in cells exposed to short-term habituation. This contrasts sharply with the reduction in both the frequency and surface area of sensory neuron active zones that accompanies long-term habituation, and suggests that modulation of active zone number and size may be an anatomical correlate that lies in the long-term domain. A quantitative analysis of the relationship between the active zone and nearby vesicle populations revealed a possible morphological substrate for the homosynaptic depression that underlies short-term habituation. Habituation leads to a depletion of synaptic vesicles immediately adjacent to the active zone. The ratio of this readily releasable pool of vesicles to the total population of vesicles associated with the active zone is 28% for control terminals, but only 11.5% for habituated terminals.(ABSTRACT TRUNCATED AT 250 WORDS)
