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Novel mechanism for non-genomic action of 17-oestradiol on kainate-induced currents in isolated rat CA1 hippocampal neurones

Qin Gu and Robert L. Moss

1. Using whole-cell voltage-clamp recordings of dissociated hippocampal CA1 neurones, we demonstrated that 17-oestradiol rapidly potentiates kainate-induced currents when applied either to the outside or the inside of the neurone. However, when the steroid was conjugated to bovine serum albumin (E₂-BSA), application to either the extracellular plasma membrane (E₂-BSA_out) or the cytosolic side of the cell (E₂-BSA_in) had no observable effect on kainate-induced currents. However, when applied stimultaneously to both sides of the plasma membrane, E₂-BSA potentiated kainate-induced currents.

2. Application of E₂-BSA_out and GTPS_in potentiated kainate-induced currents. The potentiation of kainate-induced currents by 17-oestradiol was occluded by cholera toxin pretreatment and appeared to be pertussis toxin insensitive.

3. E₂-BSA_in prolonged the effect of 8-bromoadenosine 3',5' cyclic monophosphate (8-bromo-cAMP) on kainate-induced currents. The recovery from the 8-bromo-cAMP response was found to be a function of the concentration of E₂-BSA_in. The application of ATPS_in occluded the effect of 17-oestradiol.

4. These results suggest that the non-genomic action of 17-oestradiol in the potentiation of kainate-induced currents is mediated via an action on G_s protein-coupled receptors. This operates in concert with an internal action of 17-oestradiol on a cAMP-dependent phosphorylation.

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