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1 Psychology, University of Otago, Dunedin, Otago, New Zealand
2 Anatomy and Structural Biology, University of Otago, Dunedin, Otago, New Zealand
* To whom correspondence should be addressed. E-mail: direland{at}psy.otago.ac.nz.
Group I metabotropic glutamate receptor (mGluR) agonists increase the excitability of hippocampal CAl pyramidal neurons via depression of the post-spike afterhyperpolarization. In adult rats this is mediated by both mGluR1 and mGluR5, but the signal transduction processes involved are unknown. In this study, we investigated whether altered levels of tyrosine phosphorylation of proteins is involved in the depression of the slow-duration afterhyperpolarization (sAHP) by the Group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) in CA1 pyramidal neurons of rat hippocampal slices. Preincubation with the tyrosine kinase inhibitors lavendustin A or genistein, or the Src-specific inhibitor PP2, did not inhibit the DHPG-mediated depression of the sAHP. However, preincubation with the tyrosine phosphatase inhibitor orthovanadate reduced the effects of DHPG. This effect of orthovanadate was prevented by simultaneous inhibition of tyrosine kinases with lavendustin A. Selective activation of either mGluR1 or mGluR5 by application of DHPG plus either the mGluR5 antagonist MPEP or the mGluR1 antagonist LY367385 demonstrated that the effect of inhibiting tyrosine phosphatases is not specific to either subtype of mGluR. These results suggest that the depression of the sAHP induced by activation of mGluR1 and mGluR5 is gated by a balance between tyrosine phosphorylation and dephosphorylation.
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