A study was conducted to find the effects of chronic alcohol (EtOh) administration on the rat dorsal root ganglion (DRG) cells in vivo. Morphoquantitative changes of the cytoplasmic organelles in neurons and satellite cells (SC) of lumbar DRG of animals fed with 20 and 40% of EtOH for 6 months were determined at the electron microscopic level. Stereological methods were used to quantitatively evaluate the changes in the neuronal Golgi fields, in the lysosomal system components called dense bodies (DB), in the mitochondria, and in the cytoplasmic perikaryal projections (PP) characteristic of DRG neurons. Prolonged consumption of 20% EtOh was well tolerated by neurons. There were, however, some structural modifications in the studied organelles, and there was a significant increase in the neuronal surface. In SC the number of mitochondria and DB increased significantly. Treatment with 40% EtOH produced massive organelle alterations in both neurons and SC, including disruption of the PP, markedly reducing the neuronal surface area. The architecture of the SC sheath appeared disorganized. The alterations resembled those of senescence, and indicated that a high dose of EtOH (or its metabolites) had a profound disruptive effect on the organelles and on the membrane systems of the DRG cells. The SC of the DRG units from the animals fed with EtOH were the first to show significant morphological alterations. When the architecture of the SC sheath already showed evident signs of disorganization, the neuronal body was just beginning to show morphological damage. These results suggest that the progressive disorganization of the SC sheath is a probable source of complication in peripheral neuropathy.
|Titolo:||Ultrastructural study of the alterations in spinal ganglion cells of rats chronically fed on ethanol|
|Autori interni:||BIANCHI, ROSSELLA (Ultimo)|
|Parole Chiave:||Ethanol; Neurons; Rat; Satellite cells; Spinal ganglia|
|Data di pubblicazione:||1998|
|Appare nelle tipologie:||01 - Articolo su periodico|
File in questo prodotto:
- PubMed Central loading...