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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 78 (1982), S. 19-22 
    ISSN: 1432-2072
    Keywords: Alcohol ; Trimethyltin ; Quinine ; Oral consumption of alcohol ; Polydipsia ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Male rats of the Long-Evans strain were divided into two equal groups of nine each and given either 7.0 mg/kg trimethyltin (TMT) or 0.9% saline by intragastric gavage. The pattern of self-selection of alcohol in concentrations of 3%–30% was examined in both groups at 21 and 150 days following the gavage. The TMT-treated rat consistently drank less alcohol that did the controls at every concentration of alcohol. This difference in alcohol intake was equally significant when the rats were tested in a foodcontigent, schedule-induced polydypsia situation. Further, although the TMT-lesioned animal consumed fewer calories per day in the form of alcohol, their overall daily caloric intakes were slightly higher than those of the controls. These results are interpreted as a consequence of damage to structures of the forebrain and as part of a syndrome of behavioral and neurological pathology.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 45 (1989), S. 436-443 
    ISSN: 1420-9071
    Keywords: Alcohol ; brain ; tetrahydropapaveroline ; drinking ; opiate receptors ; dopamine ; beta-carboline ; aldehyde adducts ; tetrahydroisoquinolines ; ethanol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Two classes of amine-aldehyde adducts, the tetrahydroisoquinoline (TIQ) and beta-carboline (THBC) compounds, have been implicated in the mechanism in the brain underlying the addictive drinking of alcohol. One part of this review focuses on the large amount of evidence unequivocally demonstrating not only the corporeal synthesis of the TIQs and THBCs but their sequestration in brain tissue as well. Experimental studies published recently have revealed that exposure to alcohol enhances markedly the endogenous formation of condensation products. Apart from their multiple neuropharmacological actions, certain adducts when delivered directly into the brain of either the rat or monkey, to circumvent the brain's blood-barrier system, can evoke an intense and dose-dependent increase in the voluntary drinking of solutions of alcohol even in noxious concentrations. That the abnormal intake of alcohol is related functionally to opioid receptors in the brain is likely on the basis of several dinstinct lines of evidence which include: the attenuation of alcohol drinking by opioid receptor antagoists; binding of a TIQ to opiate receptors in the brain; and marked differences in enkephalin values in animals genetically predisposed to the ingestion of alcohol. Finally, it is proposed that the dopaminergic reward pathways which traverse the meso-limbic-forebrain systems of the brain more than likely constitute an integrative anatomical substrate for the adduct-opioid cascade of neuronal events which promote and sustain the aberrant drinking of alcohol.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 98 (1989), S. 176-182 
    ISSN: 1432-2072
    Keywords: Alcohol ; Drinking ; Ro 4-4602 ; Benserazide ; Brain ; l-dopa ; Cerebral ventricle ; Dopa-decarboxylase inhibition ; Ethanol ; CNS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Following the stereotaxic implantation of chronic cannulae for intracerebroventricular (ICV) infusion, rats were given an alcohol preference test to establish their preferred concentration in comparison with water. After alcohol was removed, 15 mg/kg cyanamide was then injected subcutaneously for 4 days in order to maximize volitional intake of single solutions of alcohol, which in these animals ranged from 7 to 15%. The l-dopa-decarboxylase inhibitor benserazide (Ro 4-4602) injected subcutaneously twice daily in doses of 50–100 mg/kg failed to alter the rats' alcohol consumption either in terms of g/kg or proportional values. However, when given ICV twice daily in concentrations of 10 ng–2.0 μg per 5.0 μl volume, benserazide attenuated the rats' alcohol drinking significantly. This reduction occurred in a dose-dependent manner in terms of both absolute and proportional intakes of alcohol. Pre-treatment of the animals with 1.0 μg benserazide given ICV, when alcohol was removed from the test situation, did not abolish the subsequent ingestion of alcohol but its peripheral administration (50 mg/kg) enhanced drinking. These results suggest that the interference with the metabolic pathway of dopamine or serotonin synthesis, possibly through the mechanism of reduced formation of aldehyde adducts in the brain, markedly alters the pattern of voluntary drinking in the rat. Alternatively, benserazide could act by its central inhibition of aldehyde dehydrogenase, which in turn would concomitantly elevate levels of acetaldehyde and thereby reduce alcohol drinking.
    Type of Medium: Electronic Resource
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