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Novel mechanism for non‐genomic action of 17β‐oestradiol on kainate‐induced currents in isolated rat CA1 hippocampal neurones
Author(s) -
Gu Qin,
Moss Robert L.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.745bv.x
Subject(s) - kainate receptor , biophysics , chemistry , hippocampal formation , long term potentiation , extracellular , biochemistry , receptor , endocrinology , medicine , biology , ampa receptor , nmda receptor
1 Using whole‐cell voltage‐clamp recordings of dissociated hippocampal CA1 neurones, we demonstrated that 17β‐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 (E 2 ‐BSA), application to either the extracellular plasma membrane (E 2 ‐BSA out ) or the cytosolic side of the cell (E 2 ‐BSA in ) had no observable effect on kainate‐induced currents. However, when applied stimultaneously to both sides of the plasma membrane, E 2 ‐BSA potentiated kainate‐induced currents. 2 Application of E 2 ‐BSA out and GTPγS in potentiated kainate‐induced currents. The potentiation of kainate‐induced currents by 17β‐oestradiol was occluded by cholera toxin pretreatment and appeared to be pertussis toxin insensitive. 3 E 2 ‐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 E 2 ‐BSA in . The application of ATPγS in occluded the effect of 17β‐oestradiol. 4 These results suggest that the non‐genomic action of 17β‐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 17β‐oestradiol on a cAMP‐dependent phosphorylation.