Add time:08/14/2019         Source:sciencedirect.com

Several drugs selective for the serotonin 5-HT2A receptor were tested for their effects on spontaneous and K+-evoked [3H]γ-aminobutyric acid (GABA) release from slices of rat frontal cortex. Under K+ stimulation, the antagonists ketanserin, spiperone, R-(+)-α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenethyl)-4-piperidinemethanol (MDL 100,907) and ritanserin inhibited GABA release by 12–31%. Rats were treated with the serotonin-depleting agent para-chlorophenylalanine and with the serotonergic neurotoxin para-chloroamphetamine. In para-chlorophenylalanine-treated animals, stimulated GABA release in the presence of ketanserin remained depressed. In animals treated with both para-chlorophenylalanine and para-chloroamphetamine, ketanserin or the hallucinogenic agonist (2,5-dimethoxy-4-iodophenyl)-2-aminoethane (2C-I) each appeared to decrease stimulated GABA release but this was not significant. However, when ketanserin and 2C-I were both present in the superfusion buffer an additive inhibitory effect was observed, and GABA release was decreased 30%. These results suggest that serotonin facilitates GABA release in cortex via 5-HT2A receptors and that the functional response of this system is resistant to serotonin depletion.

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