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Effect of Ethanol on γ‐Aminobutyric Acid and Glycine Receptor‐Coupled Cl − Fluxes in Rat Brain Synaptoneurosomes
Author(s) -
Engblom A. C.,
Akerman K. E. O.
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb03764.x
Subject(s) - strychnine , picrotoxin , aminobutyric acid , chemistry , glycine receptor , glycine , taurine , ethanol , chloride , biophysics , gabaa receptor , fluorescence , receptor , biochemistry , amino acid , biology , physics , organic chemistry , quantum mechanics
Chloride fluxes in Synaptoneurosomes in response to additions of γ‐aminobutyric acid, glycine, and ethanol were measured using a chloride‐sensitive fluorescent probe 6‐methoxy‐ N ‐(3‐sulfopropyl) quinolinium (SPQ). The C1 − gradient was directed outward by bathing cells in a medium low in C1 − concentration. The Synaptoneurosomes responded to both γ‐aminobutyric acid and glycine by outflow of C1 − ions, as judged from an increase in SPQ fluorescence. These effects were inhibited by picrotoxin and strychnine, respectively. Ethanol also produced an outflow of C1 − ions from the Synaptoneurosomes. Both picrotoxin and strychnine inhibited this effect. When the antagonists were used together, the inhibiting effect was additive. These results indicate that ethanol affects both γ‐aminobutyric acid and glycine receptor‐linked chloride fluxes in the rat brain.