Meeting Abstract
The 41 amino acid peptide CRF reduces food intake and related behaviors by acting on tectal CRFR1 receptors in the African clawed frog Xenopus laevis . Precisely how CRF acts within the optic tectum to inhibit food intake is unclear but may involve inhibitory GABAergic interneurons. We predicted that if tectal CRFR1-induced inhibition of food intake is mediated via inhibitory GABAergic interneurons, that exogenous CRF would increase basal and evoked GABA release from tectal explants in-vitro. Tectal explants from X. laevis were depolarized with 60 mM K+ and GABA was measured in the medium after derivatization using high-performance liquid chromatography coupled to electrochemical detection. GABA secretion from X. laevis tectal explants increased under depolarizing conditions and this evoked release was eliminated in calcium-free medium. Exposure of tectal explants to ovine CRF doses ranging from 1 nM to 1 micromolar (AnaSpec, Inc., Fremont, CA; 0, 0.001, 0.01, 0.1, 1 µM) had no effect on either basal or depolarization-induced GABA release. We conclude that our in-vitro assay measures calcium-dependent evoked GABA release from tectal explants and that CRF does not appear to influence basal or evoked GABA release in-vitro. These findings do not support a role for GABAergic interneurons in mediating tectal CRFR1 inhibition of food intake. Supported by a grant National Science Foundation IOS #1656734.
