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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 39 (1982), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of inhibitors of γ-aminobutyric acid (GABA) metabolism or uptake on GABA output from the cerebral cortex was studied by means of a collecting cup placed on the exposed cortex of rats anaesthetized with urethane. GABA was identified and quantified by a mass-fragmentographic method. Ethanolamine-O-sulphate (10−2M) applied directly on the cerebral cortex caused a long-lasting twofold increase in GABA output, whereas dl-2, 4-diaminobutyric acid (5 × 10−3M) caused a sevenfold increase and β-alanine was inactive. The results indicate that glial uptake has little effect on GABA inactivation in the cerebral cortex. The inhibition of neuronal uptake seems a more effective tool to increase GABA concentration in the synaptic cleft, and consequently also in GABA output, than the inhibition of GABA metabolism.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Dopamine ; Yawning ; Autoreceptors ; LY 171555 ; SKF 38393
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of concurrent D-1 receptor stimulation by SKF 38393 on the expression o yawning elicited by D-2 receptor stimulation with LY 171555 was studied in the rat. A low dose of SKF 38393 (2.5 mg/kg SC), while failed to elicit yawning, potentiated the effectiveness of LY 171555 in eliciting yawning at all the doses tested (12.5, 25 and 50 μg/kg SC) and this effect was abolished by SCH 23390 (0.012 mg/kg SC). The results indicate that in analogy with typical post-synaptic dopaminergic effects (hypermotility-stereotypy), yawning elicited by a D-2 agonist is facilitated by concurrent stimulation of D-1 receptors and therefore is consistent with previous evidence that yawning in response to a D-2 agonist is not mediated by autoreceptors.
    Type of Medium: Electronic Resource
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