The effects of the loss of target cells upon photoreceptor inputs in the fly's optic lobe.

Abstract

The sensitivity of sensory neurons to target cell denervation varies in the CNS. We have examined the effects of surgically interrupting the output axons of the first optic neuropil, or lamina, in the optic lobe of the fly (Musca domestica), upon the receptor terminal inputs to the lamina. Two of the output interneurons are the monopolar cells L1 and L2, which are found as a pair in each of the unit modules or cartridges of the lamina neuropil. The lamina axons of L1 and L2 degenerate rapidly (within 0.5 h) in a retrograde direction from their lesion site, but there is no sign of retrograde transneuronal degeneration to the receptor terminals, across the input synapse. At each of these synaptic sites, L1 and L2 are invariable contributors to two of the four elements of a postsynaptic tetrad. Not only do the receptor terminals persist, but the presynaptic ribbons at the tetrad sites do also, opposite the degenerated spines of L1 and L2, indicating their lack of target dependence at least over the longest period of post-lesion recovery (48 h) examined. The areal density of presynaptic sites was conserved in the face of the degenerative loss of L1 and L2, as were the numbers of capitate projections (glial invaginations into receptor terminals). The stability of both synaptic density and capitate projection number indicates that they are predominantly influenced by the receptor terminals, which are still intact. A reduction in the number of mitochondrial profiles was one of the few observed changes in the receptor terminals. The results reflect the autonomy which the terminals have, during development, from their interneurons; they especially reflect the role of the terminals in the adult, in maintaining the presynaptic site of their afferent synapses, the tetrads.