The early causal influence of cell size upon synaptic number: the mutant gigas of Drosophila

J Neurogenet. 1994 Jul;9(3):157-76. doi: 10.3109/01677069409167277.

Abstract

The number of synaptic contacts formed by a neuron is known to vary with its surface area. This could be because large neurons are able to establish more synaptic sites, or because those neurons that are able to establish more sites are subsequently able to enlarge. To test between these two possibilities clones of enlarged ommatidia were generated in the retina of the Drosophila mutant gigas, by mitotic recombination following gamma-irradiation in the third-instar larva. The numbers of afferent synaptic contacts formed by the photoreceptor terminals in the first optic neuropil, or lamina, were then counted in the adult. The terminals of mutant photoreceptors were also enlarged, but by varying degrees. The sizes of their profiles in single sections merged with the size distribution of terminals having a wild-type phenotype, lying outside the clone in the same lamina. A perimeter of 6.0 microns for the profiles of receptor terminal in cross section was established as a criterion for distinguishing between normal and mutant phenotypes. The mutant terminals had more presynaptic sites. Because only the gigas terminals are mutant and because they enlarged at a time long before synapse formation occurred in the lamina we may conclude that cell enlargement preceded elevated synaptic number. The increase in synaptic number roughly matched the increased membrane surface of the terminals, so as nearly to preserve a constant areal density of synaptic sites over a 5-fold range in synaptic frequency.

Publication types

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

MeSH terms

  • Animals
  • Cornea / ultrastructure
  • Crosses, Genetic
  • Drosophila / genetics*
  • Drosophila / ultrastructure
  • Female
  • Gamma Rays
  • Genotype
  • Homozygote
  • Male
  • Microscopy, Electron
  • Microscopy, Electron, Scanning
  • Mosaicism
  • Mutagenesis*
  • Nerve Endings / ultrastructure
  • Neurons / cytology*
  • Neurons / ultrastructure
  • Phenotype
  • Recombination, Genetic
  • Synapses / ultrastructure*