Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9429207 | Neuroscience Letters | 2005 | 4 Pages |
Abstract
The ionophore function of γ-aminobutyric acid A (GABAA) receptors was studied by whole-cell patch clamp electrophysiology in primary cultures of rat cerebellar cortex. Chloride currents elicited by 1 μM GABA were potentiated by allopregnanolone with a plateau of high affinity (EC50 = 14 nM) and a peak of potentiation around 1 μM allopregnanolone. Furosemide (0.1 mM) eliminated the high affinity phase and increased the EC50 to 685 nM. GABAA receptors of rat cerebellar synaptosomal membranes were labelled with [3H]ethynylbicycloorthobenzoate (EBOB). Allopregnanolone displaced [3H]EBOB binding with IC50 = 320 nM. The displacing potency of allopregnanolone was strongly enhanced (IC50 = 39 nM) in the presence of 400 nM GABA and 60 nM SR 95531. Nanomolar potentiation by allopregnanolone can be associated with cerebellar GABAA receptors containing α6, β2-3 and δ subunits. This might be suitable for physiological modulation of tonic inhibitory neurotransmission via extrasynaptic GABAA receptors in cerebellar granule cells by neurosteroids.
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Authors
László Fodor, TÃmea BÃró, Gábor Maksay,