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Acute oral administration of ethanol (3.2g/kg) to rats increased (DOPAC) levels in the caudate nucleus, but had no effect on DOPAC levels in the substantia nigra and frontal cortex and failed to modify dopamine content in any of the above areas. On the other hand, the administration of the same dose of ethanol to rats which had been chronically treated with ethanol (3.2g/kg daily for 60 days), produced a decrease of DA content and a parallel increase of DOPAC levels in all areas studied. In chronically treated rats, 24 hrs after last ethanol administration dopamine levels in the frontal cortex were 60% higher than in controls. The results suggest that ethanol administration causes dopamine release in different brain areas.

AbstractNon‐adaptive activation of dopamine transmission in the nucleus accumbens shell by drugs of abuse has been attributed a fundamental role in the mechanism of drug addiction. In order to test this hypothesis, we compared in the same subject the effect of an addictive drug (ethanol) and of taste stimuli, including ethanol's own taste, on dialysate dopamine in the nucleus accumbens shell as an estimate of dopamine transmission and on taste reactivity as an expression of motivational valence. Ethanol was also monitored in the dialysates. In naive rats, intraoral infusion of a 20% sucrose + chocolate solution elicited a monophasic increase of dialysate dopamine immediately after the intraoral infusion. In contrast, intraoral infusion of 10% ethanol, 10% ethanol + 20% sucrose or 10% ethanol + 20% sucrose + chocolate solutions elicited a biphasic increase of nucleus accumbens dopamine with an early taste‐related rise and a late rise related to dialysate ethanol. Pre‐exposure to the ethanol solutions 24 h before resulted in the absence of the early dopamine rise and permanence of the late dopamine rise. This late dopamine rise was actually increased as compared with that of the nonpre‐exposed group when sucrose‐containing ethanol solutions were tested. The results indicate that single trial pre‐exposure to the ethanol solutions differentially affects the responsiveness of nucleus accumbens shell dopamine to the direct intracerebral action of ethanol and to the effect of its taste with potentiation, or no change of the first and abolition of the second. These observations point to the existence of major differences in the adaptive regulation of nucleus accumbens dopamine transmission in the shell after drug as compared with taste reward. These differences, in turn, are consistent with a role of nucleus accumbens shell dopamine in the mechanism of the behavioural effects of addictive drugs.

Neurotrophic factors, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are known to play a crucial role in growth, differentiation and function in a variety of brain neurons during development and in adult life. We have recently shown that environmental changes, aggressive behavior and anxiety-like responses alter both circulating and brain basal NGF levels. In the present review, we present data obtained using animal models which suggest that neurotrophic factors, particularly NGF and BDNF, might be implicated in mechanism(s) leading to a condition associated with schizophrenic-like behaviors. The hypothesis that neurotrophins of the NGF family can be implicated in some maldevelopmental aspects of schizophrenia is supported by findings indicating that the constitutive levels of NGF and BDNF are affected in schizophrenic patients.

The aim of this study was to evaluate the efficacy and tolerability of the DHP Ca2+ antagonist nimodipine in human AWS and post-AWS. Ten hospitalized alcoholics of both sexes with a diagnosis of AWS according to the DSM-III criteria were treated for 3 weeks in monotherapy with nimodipine p.o. at flexible daily dosages. Evaluation of AWS symptoms was performed at baseline and after 3, 5, 7, 10, 14 and 21 days. A statistically significant improvement of AWS was seen at evaluation on day 3, particularly in neurovegetative and psychopathological symptoms, and lasted up to the end of the study. The treatment was well tolerated and no side effects were observed or reported. In this pilot, open study nimodipine proved effective in the treatment of mild-to-moderate AWS. If these data are confirmed in a double-blind study nimodipine could be a rational alternative to benzodiazepines in the treatment of AWS.

The present report shows that at micromolar concentrations ethanol, like glutamate and glycine, positively modulates [ 3 H]MK-801 binding in rat cortical membranes. Very high ethanol concentrations, however, negatively modulate [ 3 H]MK-801 binding. Cerebral cortices from male Sprague-Dawley rats (200-250 g) were dissected

In unanesthetized rats the intravenous administration of low doses of ethanol (0.125-0.5 g/kg) produced a dose-dependent increase (30-80%) in the firing rate of dopaminergic (DA) neurons in the Ventral Tegmental Area (VTA). In agreement with previous observations, a dose range between 0.5 and 2 g/mg of ethanol was needed to produce comparable stimulant responses in DA neurons of the Substantia Nigra Pars Compacta. However, in anesthetized rats, doses of ethanol up to 1 g/kg failed to activate VTA-DA neurons. The high sensitivity of VTA-DA neurons to ethanol activation suggests that they might be involved in the reinforcing properties of the drug.

It has been proposed that brain catalase plays a role in the modulation of some psychopharmacological effects of ethanol. The acute administration of lead acetate has dcmonstrated a transient increase in several antioxidant cell mechanisms, including catalase. In the present study, we investigated the effects of acute lead acetate administration on ethanol‐induced behavior, brain catalase activity, and the relation between both effccts. Lead acetate (100 mgkg) or saline was injected intraperitoneally in mice. At different intervals of time (1.3, 5, 7, 9, or 11 days) after this treatment, ethanol (2.5 g/kg) was injected intraperitoneally and the mice were placed in open field chambers. Results indicated that the locomotor activity induced by ethanol was significantly increased. Maximum ethanol‐induced locomotion increase (70% more activity than control animals) was found in animals treated with lead acetate 7 days before ethanol administration. Total brain catalase activity in lead‐pretreated animals also showed a significant induction, which was maximum 7 days after lead administration. A significant correlation was found between both effects of locomotor and catalase activity. In a second study, the effect of lead administration on d‐amphetamine (2.0 mg/kg) and tert‐butanol‐ (0.5 g/kg) induced locomotor activity was investigated. Lead acetatc treatment did not affect the locomotion induced by these drugs. These data suggest that brain catalase is involved in cthanol's effects. They also provide furthcr support for the notion that acetaldehyde may be produced directly in the brain via catalase and that it may be a factor mediating some of ethanol's central effects.