After synapse formation in Drosophila, the NCAM-like molecule, fasciclin II (Fas II), is localized in both pre- and postsynaptic structures, where it controls synapse stabilization. In Fas II null mutants, synapse formation is normal, but boutons then retract during larval development. Synapse elimination and resulting lethality are rescued by transgenes that drive Fas II expression both pre- and postsynaptically. Driving Fas II expression on either side alone is insufficient31. The increase in number of synapses evoked by enhanced synaptic activity in eag Shaker and dunce mutants is accompanied by a 50% decrease of presynaptic
Fas II expression. This decrease is necessary and sufficient for presynaptic sprouting: Fas II mutants that have decreased Fas II levels by approximately 50% have sprouting similar to eag Shaker and dunce, while transgenes that maintain wild-type synaptic Fas II levels suppress sprouting in eag Shaker and dunce31. However, Fas II mutants that cause a 50% increase in bouton number do not alter synaptic strength; rather evoked release from single boutons has a reduced quantal content, suggesting that the wild-type amount of release machinery is distributed throughout more boutons32.
In Aplysia, the serotonin-induced long-term facilitation of synaptic efficacy is accompanied by the growth of new synaptic connections and downregulation of apCAM. Within 1 h, serotonin led to a more than 50% reduction of apCAM due to its internalization33. Despite the overall decline in apCAM, there is an increase of apCAM expression at postsynaptic sites where new varicosities form following treatment with serotonin. Antibodies to apCAM block these structural and functional changes. Internalization of apCAM at the surface membrane of the sensory neuron depends on MAPK phosphorylation, which, thus, represents an early regulatory step in the growth of new synaptic connections that accompanies long-term facilitation34.
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