Modulation of GABA-augmented norepinephrine release in female rat brain slices by opioids and adenosine

GABAA receptor activation augments electrically-stimulated release of norepinephrine (NE) from rat brain slices. Because this effect is not observed in synaptoneurosomes, GABA probably acts on inhibitory interneurons to disinhibit NE release. To determine whether opioids or adenosine influence GABA-...

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Bibliographic Details
Published in:Neurochemical research 2001-07, Vol.26 (7), p.853-858
Main Authors: FIBERS, Jeannie M, ETGEN, Anne M
Format: Article
Language:English
Subjects:
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology
Adenosine - pharmacology
Animals
Biological and medical sciences
Brain - drug effects
Brain - metabolism
Central nervous system
Central neurotransmission. Neuromudulation. Pathways and receptors
Electric Stimulation
Enzyme Inhibitors - pharmacology
Female
Frontal Lobe - drug effects
Frontal Lobe - metabolism
Fundamental and applied biological sciences. Psychology
gamma-Aminobutyric Acid - pharmacology
Hypothalamus - drug effects
Hypothalamus - metabolism
In Vitro Techniques
Narcotics - pharmacology
Norepinephrine - antagonists & inhibitors
Norepinephrine - metabolism
Parietal Lobe - drug effects
Parietal Lobe - metabolism
Rats
Rats, Sprague-Dawley
Vertebrates: nervous system and sense organs
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Summary:GABAA receptor activation augments electrically-stimulated release of norepinephrine (NE) from rat brain slices. Because this effect is not observed in synaptoneurosomes, GABA probably acts on inhibitory interneurons to disinhibit NE release. To determine whether opioids or adenosine influence GABA-augmented NE release, hypothalamic and cortical slices from female rats were superfused with GABA or vehicle in the presence and absence of 10 microM morphine or 100 microM adenosine. GABA augments [3H]NE release in the cortex and hypothalamus. Morphine alone has no effect on [3H]NE release, but attenuates GABA augmentation of [3H]NE release in both brain regions. Adenosine alone modestly inhibits [3H]NE release in the cortex, but not in the hypothalamus. Adenosine inhibits GABA-augmented [3H]NE release in both brain regions. The general protein kinase inhibitor H-7, augments [3H]NE release in both brain regions and may have additive effects with GABA in cortical slices. These results implicate opioid and adenosine interneurons and possibly protein kinases in regulating GABAergic influences on NE transmission.
ISSN:0364-3190
1573-6903
DOI:10.1023/A:1011676505575