Ethanol dependence and withdrawal selectively alter localized cerebral glucose utilization.

The 2-deoxyglucose technique was used to determine local cerebral glucose utilization (LCGU) in over 50 brain regions of rats physically dependent upon ethanol and compared to those of acutely intoxicated and those undergoing an overt ethanol-withdrawal syndrome. Dependent-intoxicated rats (average blood ethanol concentration 64 mM) had decreased LCGU in 13/54 regions, including those associated with the limbic system, cerebellum, and motor system. The ethanol withdrawal syndrome was associated with 17/50 gray regions showing an increase, including regions involved with motor function, auditory system, and mammillary bodies-anterior thalamus-cingulate cortex pathway.

A comparison of calcium antagonists and diazepam in reducing ethanol withdrawal tremors.

The calcium antagonists nimodipine and dantrolene were compared with diazepam in an animal model of tolerance and physical dependence upon ethanol. Nimodipine and dantrolene were both effective in suppressing withdrawal tremors but diazepam was clearly superior to both agents. These results suggest that the ethanol withdrawal syndrome is only partially mediated by increased calcium flux.

Acute ethanol administration selectively alters localized cerebral glucose metabolism.

The effects of acute ethanol administration on glucose utilization in the CNS of rat were studied using the 2-deoxyglucose technique. Cerebral glucose utilization was determined for 53 brain regions at peak and descending blood ethanol concentrations averaging 14, 26 and 66 mM. Decreased glucose utilization was the predominant finding and was observed in 20% of the regions evaluated, with median raphe, vestibular nucleus, cerebellar vermis, and various structures associated with the auditory system showing the greatest reductions.

Actions of ethanol on voltage-sensitive sodium channels: effects of acute and chronic ethanol treatment.

The effects of acute and chronic ethanol treatment on neurotoxin-stimulated 22Na+ uptake and [3H]batrachotoxinin A20-alpha-benzoate binding to neuronal sodium channels were studied in rat forebrain synaptosomes. Fluorescence measurements were used to assess the intrinsic order or fluidity and the sensitivity to ethanol of rat forebrain synaptic plasma membranes at various intervals during and after chronic ethanol treatment. Acute ethanol administration had no significant effect on neurotoxin binding in the absence or presence of ethanol in vitro or on sodium uptake in the absence of ethanol in vitro.

Influence of thiamine deficiency on the response to ethanol in two inbred rat strains.

We investigated whether thiamine deficiency (TD), a frequent concomitant of chronic alcoholism, differentially modifies the response to ethanol in two inbred rat strains with highly different genetic susceptibilities to development of TD encephalopathy. Ethanol-induced (3 g/kg i.p.