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EVOLUTION OF THE INTRACELLULAR CHANGES IN NEURONS CAUSED BY TRIMETHYLTIN
Author(s) -
BROWN A. W.,
CAVANAGH J. B.,
VERSCHOYLE R. D.,
GYSBERS M. F.,
JONES H. B.,
ALDRLDGE W. N.
Publication year - 1984
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1984.tb00359.x
Subject(s) - golgi apparatus , endoplasmic reticulum , biology , hippocampal formation , microbiology and biotechnology , pyramidal cell , anatomy , neuroscience
Rats have been given a single dose of trimethyltin (10 mg/kg) and the intracellular events have been followed particularly in hippocampus, cerebral cortex, cerebellum and spinal ganglion cells. The earliest change visible occurs 12 h after this dose and is found to be dense membrane‐bound bodies, probably derived from branching tubulo‐vesicular smooth endoplasmic reticulum formations. These occur in close connection with rough endoplasmic reticulum and polyribosomes and appear also to have some association with the Golgi complex. At 24 h there is a general vacuolation of Golgi cisterns and SER membranes, and the membrane‐bound dense body formation is greatly increased. SER abnormalities are particularly conspicuous in Purkinje cells. In spinal ganglion cells, while vacuolation of Golgi cisterns is intense, dense bodies are inconspicuous and are replaced by increased autophagosomes, often of great complexity. By 48 h vacuolation of Golgi cisterns has waned, but accumulation of dense bodies and secondary lysosomes has steadily increased. In spinal ganglion cells autophagosomes only are increased as the Golgi vacuolation declines. At later times steady increases of lysosomal dense bodies is seen generally accompanied in hippocampal pyramidal cells and dentate fascia cells by abundant cell death. The suggestion is put forward that the Golgi complex may be the seat of the critical metabolic lesion and disturbances to protein transfer and protein synthesis follow. No explanation for the selective loss of hippocampal h 1–5 , (CA 1 ‐CA 4 except Sommer's sector) pyramidal cells and of small dentate fascia neurons can be derived from these conclusions.