GABAB-receptor mediated inhibition of potassium-evoked release of endogenous 5-hydroxytryptamine from mouse frontal cortex.
The effect of baclofen, the GABAB-agent, on the potassium-evoked release of endogenous 5-hydroxytryptamine (5-HT) from slices of mouse frontal cortex has been investigated. The release of endogenous 5-HT evoked by addition of K+ (35 mM) was inhibited by (+/-)-baclofen in a dose-dependent manner with an IC50 of 0.1 microM. Inhibition of K+-evoked release of 5-HT was produced by (+/-)- and (-)-baclofen but not (+)-baclofen. This action of the (-)-enantiomer was not altered by the presence of the (+)-enantiomer. Addition of GABA (0.1-10 microM) also induced a dose-dependent inhibition of 5-HT release. This effect was neither enhanced by flurazepam (1 microM) nor antagonized by bicuculline (10 microM). The progabide metabolite, 4-[( (4-chlorophenyl) (5-fluoro-2-hydroxyphenyl)methylene]amino)butyric acid (SL75.102) (1 microM) inhibited the K+-evoked release of 5-HT by 61%. These data suggest that baclofen is a potent inhibitor of the K+-evoked release of endogenous 5-HT from the cortex and further indicate that the release of 5-HT may be controlled by a GABAB-receptor located presynaptically.[1]References
- GABAB-receptor mediated inhibition of potassium-evoked release of endogenous 5-hydroxytryptamine from mouse frontal cortex. Gray, J.A., Green, A.R. Br. J. Pharmacol. (1987) [Pubmed]
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