Abstract
Noradrenaline release from synaptosomes of rat hippocampus is modulated by both GABA and benzodiazepines. GABAA and GABAB receptors are present on these nerve terminals, and agonists at these receptors enhance spontaneous release and depress K+ -evoked release, respectively. Chlordiazepoxide has a dual effect: it enhances the action of GABA at GABAA receptors and depresses K+ -evoked release of [3H]noradrenaline in the absence of GABA. The mechanism of these actions and their in vivo role are discussed.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcimycin / pharmacology
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Chlordiazepoxide / pharmacology
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Dose-Response Relationship, Drug
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Hippocampus / physiology*
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In Vitro Techniques
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Norepinephrine / metabolism*
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Potassium / pharmacology
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Rats
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Receptors, Cell Surface / physiology*
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Receptors, GABA-A
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Synaptosomes / metabolism
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gamma-Aminobutyric Acid / pharmacology
Substances
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Receptors, Cell Surface
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Receptors, GABA-A
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Calcimycin
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gamma-Aminobutyric Acid
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Chlordiazepoxide
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Potassium
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Norepinephrine