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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 290 (1981), S. 514-516 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Working on a series of imidazodiazepines, we found compounds which were potent inhibitors of the specific high-affinity binding of 3H-diazepam to brain synaptosomal fractions, but which failed to produce any of the behavioural and neurological effects typical of benzodiazepines. Detailed analysis ...
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 263 (1976), S. 173-174 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] BASED on a few experiments on Deiters? neurones and cerebellar Purkinje cells, Steiner and Felix1 concluded that benzodiazepines antagonise the inhibitory effect of GABA. To understand the mode of action of centrally acting agents, the evidence available from various pharmacological experiments ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 294 (1976), S. 1-7 
    ISSN: 1432-1912
    Keywords: Neuroleptics ; Benzodiazepines ; Dopamine ; HVA ; GABA ; Catalepsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several benzodiazepines (chlordiazepoxide, clonazepam, diazepam and flunitrazepam) markedly counteracted the elevation of the homovanillic acid (HVA) content of the rat brain induced by neuroleptics (haloperidol, pimozide, chlorpromazine, and clozapine). A similar effect was obtained with the inhibitor of GABA transaminase, aminooxyacetic acid (AOAA). The interaction of benzodiazepines with the neuroleptic-induced HVA increase was similar in the striatum and in the limbic forebrain, and was antagonized by the GABA receptor-blocking agent, picrotoxin. Both the benzodiazepines used and AOAA potentiated the cataleptic effect of the four neuroleptics. It is concluded that benzodiazepines, by intensifying GABA-ergic transmission, enhance the ongoing inhibition of mesencephalic dopamine neurons exerted by the striatonigral GABA system. As a consequence, the feedback activation of dopamine neurons induced by the neuroleptic blockade of dopamine receptors in the striatum and the limbic system is attenuated. This results in a reduction of the neuroleptic-induced increase of HVA and in the potentiation of the cataleptic effect of neuroleptics.
    Type of Medium: Electronic Resource
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