Abstract |
The effects of CPA (a selective A1 receptor agonist), NECA (a mixed A1 and A2 receptor agonist), and CGS 21680 (a selective A2 receptor agonist) on the ischemia-evoked release of gamma-aminobutyric acid ( GABA) from rat cerebral cortex was investigated with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. In control animals, superfusate GABA increased from a basal level of 206 +/- 26 nM (mean +/- S.E.M., n = 18) to 10,748 +/- 3,876 nM during the reperfusion period. Pretreatment with adenosine receptor agonists failed to affect basal levels of GABA release. However, CPA (10(-10) M), NECA (10(-9) M), and CGS 21680 (10(-8) M) significantly suppressed the ischemia-evoked release of GABA. The ability to block the ischemia-evoked release of GABA was not evident when the adenosine receptor agonists were administered at higher concentrations. Thus, the selective activation of either A1 or high-affinity A2a adenosine receptors results in an inhibition of ischemia-evoked GABA release.
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Authors | M H O'Regan, R E Simpson, L M Perkins, J W Phillis |
Journal | Brain research
(Brain Res)
Vol. 582
Issue 1
Pg. 22-6
(Jun 05 1992)
ISSN: 0006-8993 [Print] Netherlands |
PMID | 1498681
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Phenethylamines
- Receptors, Purinergic
- 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine
- Adenosine-5'-(N-ethylcarboxamide)
- N(6)-cyclopentyladenosine
- gamma-Aminobutyric Acid
- Adenosine
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Topics |
- Adenosine
(analogs & derivatives, pharmacology)
- Adenosine-5'-(N-ethylcarboxamide)
- Analysis of Variance
- Animals
- Cerebral Cortex
(drug effects, metabolism)
- Dose-Response Relationship, Drug
- Electroencephalography
- Ischemic Attack, Transient
(metabolism, physiopathology)
- Kinetics
- Male
- Phenethylamines
(pharmacology)
- Rats
- Rats, Inbred Strains
- Receptors, Purinergic
(drug effects, physiology)
- Time Factors
- gamma-Aminobutyric Acid
(metabolism)
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