The effect of γ‐aminobutyric acid (GABA) and its agonists muscimol and 4,5,6,7‐tetrahydroisoxazolo(5‐4‐c)pyridin‐3‐ol (THIP) on the development of GABA receptors on cerebellar granule cells was studied by cultivation of the cells in media containing these substances. It was found that the presence of 50 μM GABA in the culture media led to the induction of low‐affinity GABA receptors (KD 546 ± 117 nM) in addition to the high‐affinity receptors (KD 7 ± 0.5 nM) which were present regardless of the presence of GABA in the culture media. The functional activity of the GABA receptors was tested by investigating the ability of GABA to modulate evoked glutamate release from the cells. It was found that GABA could inhibit evoked glutamate release (ED50 10 ± 3 (μM) only when the cells had been cultured in the presence of 50 νM GABA, 50 μM muscimol, or 150 μM THIP, i.e., under conditions where low‐affinity GABA receptors were present on the cells. This inhibitory effect of GABA could be blocked by 120 μM bicuculline and mimicked by 50 μM muscimol or 150 μM THIP whereas 150 μM (‐)‐baclofen had no effect. It is concluded that GABA acting extracellularly induces formation of low‐affinity receptors on cerebellar granule cells and that these receptors are necessary for mediating an inhibitory effect of GABA on evoked glutamate release. The pharmacological properties of these GABA receptors indicate that they belong to the so‐called GABAA receptors.
Journal of Neurochemistry – Wiley
Published: Dec 1, 1984
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