Abstract
The present work is an extension of a previous study concerning the effect of ethanol withdrawal on brain mitochondria. It was shown earlier that ethanol withdrawal induced an increase in permeability of mitochondria to phenazine methosulfate (PMS). This was measured indirectly by the SDH-PMS assay. In a pilot study chlorpromazine (CPZ) in vitro reversed the ethanol withdrawal effect. In the present study it was shown that mitochondria enclosed within the synaptosomal cytoplasm and plasma membrane also developed an increase in permeability to PMS. This suggested that the permeability change may also exist within the intact brain. To further test this idea two drugs known to be effective in the treatment of delirium tremens were given to the ethanol withdrawal rats in vivo. Their effect on the ethanol withdrawal mitochondria change was compared with the effect of adding pharmacologically active concentrations of ethanol and CPZ in vitro. Ethanol and CPZ both in vivo and in vitro restored the mitochondrial permeability barrier to control levels. These results are indirect evidence that the ethanol withdrawal mitochondrial abnormality may have an etiologic genesis in common with ethanol dependency symptomatology.
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