초록 일부
Alcohol is the most used psychiotropic drug. It is well known that long-term heavy alcohol(ethanol) intake causes alcoholic dementia, cerebellar degeneracy or Wernicke-korsakoff Syndrome and aggravate...
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초록 전체
Alcohol is the most used psychiotropic drug. It is well known that long-term heavy alcohol(ethanol) intake causes alcoholic dementia, cerebellar degeneracy or Wernicke-korsakoff Syndrome and aggravates the conditions of many other neuro-psychotic disorders. Despite the serious problems associated with ethanol, there is little research on the
* A thesis submitted to the committee of Graduate School, Chungnam National University in partial fulfillment of the requirements for the degree of Master of Home Economics conferred in February 2000.
reaction mechanism of ethanol on the central nervous system. Recently it is indicated that PKC plays an important role in the action of ethanol and in the neuroadaptational mechanisms under chronic ethanol exposure. Accordingly this study was carried out to investigate the effect of ethanol in the range of not showing any cytotoxicity on the PKC isoform levels in B103 cells from the rat central nervous system using western blot analysis and PKC isoform-specific antibodies. The changes of PKC α, β, γ, ε and ζ level in the range of ethanol concentration 50, 100 and 200mM were examined at the exposure time 1, 2, 8, 18 and 24hrs and in both fractions (cytosolic and membrane fraction).
PKC α turned out to be decreased in the cytosolic fraction at 1, 2 and 8hrs ethanol exposure times in all the ethanol concentrations but increased in both cytosolic and membrane fractions at 24hr ethanol exposure time in 200mM ethanol concentration. PKC β was not detected, however PKC γ was significantly decreased in both cytosolic and membrane fractions at 24hr ethanol exposure time in all the ethanol concentrations. PKC ε was decreased at all the ethanol exposure times in all the ethanol concentrations in the cytosolic fraction and at 24hr ethanol exposure time in any ethanol concentrations, the trend of decreased was observed in the membrane fraction. Lastly the change of PKC ζ level did not show any consistency.
These results altogether indicate that in the range of ethanol concentration not show cytotoxicity, ethanol may modulate signal transduction and neurotransmitter release in the central nervous system, through the change of PKC isoform level, and the action of these isoforms may be different each other in the cell by showing the different pattern of change according to the PKC isoform type. In addition, these results imply that the behavioral abnormality of inhibition or excitation of central nervous system caused by ethanol may appeared through the change of signal transduction system PKC involved.
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