ISSN:
1432-0878
Keywords:
Transmission and high voltage electron microscopy
;
Drosophila
;
Degeneration
;
Retinular cells
;
Optic neuropiles
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary The compound eye and the two most distal optic neuropils (lamina ganglionaris and medulla externa) of the Drosophila mutant w rdgB KS222were examined with transmission electron microscopes at conventional (60 kV) and high (0.8–1 MV) voltages. Eye tissue was sampled in the newly emerged and at 3, 7, and 21 days following eclosion. This mutant is known to show a light-induced degeneration of the peripheral retinular cells (R 1–6); the spectral sensitivity is altered and the threshold is increased reflecting the function of the central cells (R7, 8) which do not degenerate. A totally normal appearing visual system (peripheral retina and optic neuropiles) was found in newly emerged adults. After 3 days the somata of some of the peripheral retinal cells are affected and all of their axons show degeneration. At one week the R 1–6 pathology is well advanced in both somal and axonal regions. In affected cells the cytoplasm is more or less uniformly electron dense and contains liposomes, lysosome-like bodies, myeloid figures and vacuoles suggesting autophagy. Such cytoplasm (noted at 3 and 7 days post-eclosion) exhibits an electron dense reticulum and degenerate mitochondria. Microvilli become more electron dense. Retinular axon terminals are electron opaque and lack synaptic vesicles with few if any presynaptic structures. Mitochondrial remains are barely recognizable. Transsynaptic degeneration was not found. After 3 weeks, the structure of R 1–6 in the peripheral retina (somata and rhabdomeres) is greatly reduced or lost while R7 and R8 and higher order neurons are not affected. The debris from cell bodies and axon terminals of R 1–6 seems diminished, so that some phagocytosis probably takes place along with gliosis in the lamina.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00216214
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