Genetic dissection of structural and functional components of synaptic plasticity. II. Fasciclin II controls presynaptic structural plasticity

Neuron. 1996 Oct;17(4):655-67. doi: 10.1016/s0896-6273(00)80198-1.


Increased neuronal activity (eag Shaker mutants) and cAMP concentration (dunce mutants) lead to increased synaptic structure and function at the Drosophila neuromuscular junction. Here, we show that the increase in synaptic growth is accompanied by an approximately 50% decrease in synaptic levels of the cell adhesion molecule Fasciclin II (Fas II). This decrease in Fas II is both necessary and sufficient for presynaptic sprouting; FasII mutants that decrease Fas II levels by approximately 50% lead to sprouting similar to eag Shaker and dunce, while transgenes that maintain synaptic Fas II levels suppress sprouting in eag Shaker and dunce. However, FasII 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 boutons.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Cell Adhesion Molecules, Neuronal / biosynthesis
  • Cell Adhesion Molecules, Neuronal / physiology*
  • Cyclic AMP / metabolism
  • Drosophila
  • Gene Expression Regulation
  • Larva
  • Muscles / innervation
  • Mutagenesis
  • Neuromuscular Junction / physiology*
  • Neuromuscular Junction / ultrastructure
  • Neuronal Plasticity
  • Neurons / physiology*
  • Neurons / ultrastructure
  • Synapses / physiology*
  • Synapses / ultrastructure*


  • Cell Adhesion Molecules, Neuronal
  • fasciclin II
  • Cyclic AMP