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Acta Physiologica 2009; Volume 195, Supplement 669
The 88th Annual Meeting of The German Physiological Society
3/22/2009-3/25/2009
Giessen, Germany
DISRUPTION OF STIMULATION OF GLUTAMATE RECEPTORS BY A SCHIZOPHRENIA-ASSOCIATED KINASE MUTANT
Abstract number: P372
Seebohm1 G., Henrion2 U., Steinke1 K., Hollmann1 M., Lang2 F., Strutz-Seebohm1 N.
1Biochemie I, Ruhr-University Bochum, Bochum
2Physiology I, University of Tbingen, Tbingen
PIP5K2A is a kinase recently reported to be associated with schizophrenia. Several lines of evidence suggest an involvement of glutamate receptors in schizophrenia.
Here, we show that, in Xenopus oocytes coexpressing the AMPA receptor subunit GluR1 or the KA receptor subunit GluR6 with PIP5K2A, glutamate-induced currents were significantly increased. By contrast, this stimulatory effect of PIP5K2A was abolished by coexpression of the PIP5K2A(N251S) mutant with either GluR1 or GluR6. PIP5K2A produces the lipid PI(4,5)P2, which is involved in multiple cell functions. Therefore, a water soluble PI(4,5)P2 analogue was injected into oocytes expressing either GluR1 or GluR6. As expected, the putative PIP5K2A product PI(4,5)P2 induced an increase of glutamate currents. These preliminary results point to an involvement of the PIP5K2A kinase in the regulation of glutamate receptors and could provide new insights into the understanding of the complex disease of schizophrenia.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 669 :P372