Journal of Neuroscience, Vol 11, 1930-1941, Copyright © 1991 by Society for Neuroscience
Terminal degeneration and synaptic disassembly following receptor photoablation in the retina of the fly's compound eye
JH Brandstatter, SR Shaw and IA Meinertzhagen
Life Sciences Centre, Dalhousie University, Halifax, Nova Scotia, Canada.
A long-term objective of our studies on the first optic neuropil (or
lamina) underlying the fly's compound eye is to explore how afferent
photoreceptor synapses disappear during normal adult experience. To
increase the frequency of this loss and the chances for its detection
artificially, we have examined in this study the synapses during the
degeneration of their presynaptic elements, the synaptic terminals of the
receptor cells. This may be reliably procured by illuminating for 12 min
with strong green light eyes that have received an injection of the dye
sulforhodamine 101 (Picaud et al., 1988). The lesion is local and develops
rapidly. Degeneration among terminals is progressive but asynchronous.
There are several different types of degeneration, most interpretable as
stages in a temporal progression after illumination- induced injury.
Degenerative changes include shrinkage and darkening of terminals and
mitochondrial swelling. Synaptic sites are lost in a defined sequence: (1)
the T-shaped presynaptic ribbon disappears first; (2) the members of what
is normally a tetrad of postsynaptic elements withdraw as an ensemble from
the receptor terminal's membrane, and the surrounding epithelial glial
cells extend between former pre- and postsynaptic partners; and (3) the
postsynaptic elements then separate from each other. In the most rapidly
affected terminals, the frequencies for those synaptic sites at which both
presynaptic ribbons and postsynaptic elements remain intact decline by 85%,
even in the first 8 hr postillumination.