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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 473 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 7
    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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  • 8
    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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  • 9
    ISSN: 1573-6903
    Keywords: Calcium ; tetrahydropapaveroline (THP) ; salsolinol ; push-pull perfusion ; amine-aldehyde adduct ; tetrahydroisoquinoline (TIQ)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The kinetics of45Ca2+ efflux were examined at circumscribed sites in the perfused hippocampus of the freely moving rat with either one of two tetrahydroisoquinoline (TIQ) products, tetrahydropapaveroline (THP) or salsolinol. Guide tubes for unilateral push-pull perfusion were implanted stereotaxically to rest just above sites within the dorsal hippocampus. Upon recovery from surgery, a tissue site in the hippocampus was prelabeled with 1.0 μl of45Ca2+ (2.0 μCi) injected through the indwelling guide tube. After 16–20 hr had elapsed, successive push-pull perfusions of the site were carried out with an artificial cerebrospinal fluid (CSF), at 5.0 min intervals and at a rate of 20 μl/min, in order to obtain a control washout curve of declining radioactivity. On the fifth of a series of 5.0 min perfusions, either THP or salsolinol was added to the perfusion medium in a concentration of 10 or 100 ng/μl. Then the hippocampal site was perfused again with control CSF for the collection of an additional three samples. Although THP in both of the test concentrations generally augmented the efflux of45Ca2+, the temporal course and magnitude of the enhancement depended on the anatomical site of the perfusion. In the more rostral hippocampal planes of AP 3.0 and AP 4.0, THP caused a delayed efflux of the cation, after the perfusion of THP had been discontinued, in nearly half of the loci reactive to the TIQ. Similarly, salsolinol enhanced significantly the efflux of45Ca2+ in a concentration-dependent manner during the interval of its perfusion within the hippocampal plane of AP 3.0. These results suggest that both THP and salsolinol can affect differentially the kinetics of45Ca2+ efflux and that these differences are contingent on the circumscribed anatomical site of push-pull perfusion. It is envisaged that a part of the neurochemical effects of the two TIQs when acting centrally are mediated by membrane mechanisms involving Ca2+ transport, metabolism or other cellular activity of the cation.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 11 (1986), S. 1643-1651 
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the characteristics of the uptake within hypothalamic tissue of the Ca2+-channel blocker, verapamil, push-pull canulae were implanted bilaterally above the anterior hypothalamic-preoptic area (AH/POA) and posterior hypothalamus (PH) of the cat. The functional reactivity of these two anatomical regions was verified in the unrestrained cat, prior to a push-pull perfusion, by a microinjection of either 5–7 μg norepinephrine (NE) into AH/POA, or by perfusion of 50 mM Ca2+ within the PH, both of which induce a transient decline in the cat's core temperature. Verapamil was perfused in a concentration of 0.4, 2.0 or 4.0 μg/μl for successive 10 and 20 min intervals within these NE and Ca2+-sensitive sites. A quantitative analysis of verapamil in each sample of perfusate was performed double-blind by HPLC-spectrophotometric detection. The results showed that the percent recovery of verapamil after the 10 min interval was always less than that after the next 20 min period of perfusion. These recovery values were independent of the site of perfusion and the concentration of verapamil. However, the mean uptake of verapamil into tissue after 10 min was significantly greater than that after the 20 min period for all concentrations tested. These results demonstrate that the hypothalamus has a time-dependent characteristic to incorporate a Ca2+-channel blocker into the parenchyma. Once the point of tissue saturation is reached, a steady-state level of verapamil uptake is established.
    Type of Medium: Electronic Resource
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