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Vol. 288, Issue 2, 866-878, February 1999
The Psychiatric Institute, Department of Psychiatry, College of
Medicine, University of Illinois, and Psychiatry Research Service,
Veterans Administration Chicago Health Care System (West Side
Division), Chicago, Illinois
This investigation examined the effects of acute and chronic
ethanol exposure and its withdrawal on the cAMP-responsive element binding protein (CREB) and the activator protein-1 (AP-1) gene transcription factors in the rat brain. The anxiogenic effects of
ethanol withdrawal after acute or protracted ethanol treatment of rats
were measured by the elevated plus-maze (EPM) test. It was observed
that ethanol withdrawal after acute ethanol treatment has no effect on
open-arm activity (percent of open-arm entries and the mean percent of
time spent on the open arms) of rats on the EPM test. On the other
hand, the time course studies of the development of anxiety during
ethanol withdrawal (0, 12, 24, and 72 h) after 15 days of ethanol
treatment indicate that peak anxiety (significant decrease in open-arm
activity) occurred at 24 h of ethanol withdrawal in rats. It was
observed that acute ethanol treatment and its withdrawal (24 h) had no
effect on CRE- or AP-1 DNA-binding activities in the rat cortex as
determined by the electrophoretic gel-mobility shift assay. It was also
found that chronic ethanol treatment and its withdrawal (24 h) had no
effect on AP-1 DNA-binding activity in the rat cortex. Investigation of
the time course studies of changes in CRE-DNA-binding activity during
ethanol withdrawal (0, 12, 24, and 72 h) after 15 days of ethanol
treatment indicated that the peak reduction of CRE-DNA-binding activity
occurred at 24 h of ethanol withdrawal. The changes in the
immunolabeling of the CREB-related target, that is, brain-derived neurotrophic factor (BDNF), in the rat cortex during chronic ethanol treatment and its withdrawal (24 h) were examined using western blotting. It was found that 24 h but not 0 h of ethanol
withdrawal after 15 days of ethanol treatment caused a significant
decrease in the immunolabeling of BDNF in the rat cortex. Fluoxetine
(alone) treatment of rats for 1 or 15 days had no effect on open-arm
activity and cortical CRE-DNA-binding activity. However, when
fluoxetine was administered concurrently with ethanol treatment for 15 days, it caused a reversal of the anxiogenic effects of ethanol
withdrawal and antagonized the down-regulation of CRE-DNA-binding
activity and of the decrease in immunolabeling of BDNF in the cortices of ethanol-withdrawn rats. On the other hand, acute fluoxetine treatment produced normalization of the reduction of cortical CRE-DNA
binding in ethanol-withdrawn rats (24 h) but did not reach the level of
significance compared with normal control rats. Acute fluoxetine
treatment had no effect on anxiety in ethanol-withdrawn rats. Taken
together, these results suggest the possibility that decreased
CRE-DNA-binding activity in the rat cortex may be associated with the
molecular mechanisms of ethanol dependence (i.e., ethanol withdrawal-related anxiety).
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