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ADENOSINE INHIBITION OF γ‐AMINOBUTYRIC ACID RELEASE FROM SLICES OF RAT CEREBRAL CORTEX
Author(s) -
HOLLINS CAROLYN,
STONE TREVOR W.
Publication year - 1980
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1980.tb10888.x
Subject(s) - adenosine , inhibitory postsynaptic potential , chemistry , gamma aminobutyric acid , adenosine a1 receptor , theophylline , calcium , verapamil , inosine , adenosine receptor , aminobutyric acid , medicine , pharmacology , endocrinology , biochemistry , biology , receptor , agonist , organic chemistry
1 The effect of purine compounds on the potassium‐evoked release of 14 C‐labelled γ‐aminobutyric acid (GABA) has been studied in 400 μm slices of rat cerebral cortex in vitro . 2 Adenosine and adenosine 5′ monophosphate (AMP) inhibited the release of GABA at 10 −5 to 10 −3 m . Adenosine triphosphate (ATP) produced a significant inhibition of release only at 10 −3 m . 3 Theophylline 10 −4 or 10 −3 m reduced the inhibitory effect of adenosine, but did not change basal release of GABA. 4 Dipyridamole 10 −5 m itself reduced evoked GABA release, but did not prevent the inhibitory effect of adenosine, implying that adenosine was acting at an extracellularly directed receptor. 5 Calcium removal or antagonism by verapamil reduced the evoked release of GABA, but adenosine did not produce any further reduction of the calcium‐independent release. This may indicate that the inhibitory effect of adenosine on GABA release results from interference with calcium influx or availability within the terminals.