Increased GABAB receptor function in mouse frontal cortex after repeated administration of antidepressant drugs or electroconvulsive shocks.

摘要

1 Addition of baclofen to a medium containing slices of mouse frontal cortex inhibited the potassium-evoked release of 5-hydroxytryptamine (5-HT) in a concentration-dependent manner. The degree of inhibition was increased in frontal cortex tissue taken from animals treated for 14 days with amitriptyline (10 mg kg-1, twice daily) at all concentrations of baclofen tested (10(-6) M-10(-4) M). 2 Administration of either desipramine, mianserin or zimeldine (10 mg kg-1 daily) for 14 days also approximately doubled the degree of inhibition evoked by addition of baclofen (10(-5) M) to the medium. 3 One day of treatment with the antidepressant drugs did not alter the inhibitory effect of baclofen on K+-evoked 5-HT release. 4 Addition of the antidepressant drugs to the medium had no effect on the K+-evoked release of 5-HT. 5 Repeated administration of electroconvulsive shock (5 seizures spread out over 10 days), like amitriptyline, produced a significant enhancement of the baclofen-induced inhibition of 5-HT release over the range of baclofen concentrations studied. A single electroconvulsive shock had no effect. 6 These data suggest that repeated administration of the antidepressant drugs or electroconvulsive shock increases the function of the gamma-aminobutyric acid (GABA)B receptor in the frontal cortex modulating 5-HT release and are consistent with the finding of increased GABAB receptor number in this region following various antidepressant treatments.