Alcoholism, clinical and experimental research · 2006
Ethanol-related smooth endoplasmic reticulum dilation in purkinje dendrites of aging rats.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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Dlugos Cynthia A
Аннотация
BACKGROUND: Long-term ethanol consumption in aging rats results in degeneration and regression of the Purkinje neuron (PN) dendritic arbor. One marked ethanol-related change in Purkinje dendrite ultrastructure is dilation of the smooth endoplasmic reticulum (SER) within PN dendritic shafts. The purpose of this study was to determine a time course for ethanol-related dendritic regression in PN dendritic shafts and spines.
METHODS: One-hundred eighty aging, male Fischer 344 rats were used. Four durations of treatment (5, 10, 20, and 40 weeks) and 3 dietary treatment groups (60 rats/treatment group) were studied. Ethanol-fed rats received a liquid ethanol diet (35% of dietary calories from ethanol). Pair-fed rats received an isocaloric liquid control diet and chow-fed rats received rat chow and water ad libitum. After each duration of treatment, 45 rats (15/treatment) were euthanized and 2 posterior cerebellar lobules/rat were viewed with electron microscopy and photographed. Diameters of SER profiles within PN shafts and spines were measured with image analysis.
RESULTS: Ethanol-related SER dilation in dendritic shafts occurred following 40 weeks of treatment. Ethanol-related SER dilation was not detected in PN dendritic spines.
CONCLUSIONS: These results confirm that ethanol-related dilation of SER profiles in PN dendritic shafts occurs following the same duration of treatment as the dendritic regression previously reported in other studies. Degenerating bodies that may be linked to dendritic regression were also identified in PN dendrites.
METHODS: One-hundred eighty aging, male Fischer 344 rats were used. Four durations of treatment (5, 10, 20, and 40 weeks) and 3 dietary treatment groups (60 rats/treatment group) were studied. Ethanol-fed rats received a liquid ethanol diet (35% of dietary calories from ethanol). Pair-fed rats received an isocaloric liquid control diet and chow-fed rats received rat chow and water ad libitum. After each duration of treatment, 45 rats (15/treatment) were euthanized and 2 posterior cerebellar lobules/rat were viewed with electron microscopy and photographed. Diameters of SER profiles within PN shafts and spines were measured with image analysis.
RESULTS: Ethanol-related SER dilation in dendritic shafts occurred following 40 weeks of treatment. Ethanol-related SER dilation was not detected in PN dendritic spines.
CONCLUSIONS: These results confirm that ethanol-related dilation of SER profiles in PN dendritic shafts occurs following the same duration of treatment as the dendritic regression previously reported in other studies. Degenerating bodies that may be linked to dendritic regression were also identified in PN dendrites.