Rabbit Anti-Human GRIA4 (Phospho-Ser862) polyclonal antibody

C3H/HeJ mice have been reported to have relatively early onset of spike-wave discharges (SWD), and a defective AMPA receptor subunit Gria4 as the genetic cause. We investigated the time course of SWD development through serial EEG recordings in C3H/HeJ mice to better characterize this model. We found that at immature postnatal ages of 5-15 days, rare SWD-like events were observed at an average rate of 3 per hour, and with relatively broad spikes, irregular rhythm, slow frequency (5-6 Hz), and short duration (mean 1.75 s). This was followed by a transitional period of increasing SWD incidence, which then stabilized in mature animals at age 26-62 days, with SWD at an average rate of 45 per hour, narrower spike morphology, regular rhythm, higher frequency (7-8 Hz), and longer duration (mean 3.40 s). This sequence of maturational changes in SWD development suggests that effects of early intervention could be tested in C3H/HeJ mice over the course of a few weeks, rather than a few months as in rats, greatly facilitating future research on anti-epileptogenesis. (C) 2009 Published by Elsevier B.V.

The glutamatergic dysfunction hypothesis suggests that genes involved in the glutamate neurotransmitter system are candidates for schizophrenia-susceptibility genes. We have been doing systematic studies of the association of schizophrenia with each member of the glutamate receptor gene family. In this review, we summarize our results of association studies of five glutamate receptor genes, two of which are metabotropic, GRM2 and GRM3, whereas the other four are ionotropic, GRIA4, GRIK1, GRIK2 and GRIM. Haplotype analyses using combinations of SNPs evenly distributed across the relevant genes showed significant associations of GRM3 and GRIA4 with schizophrenia. We discuss the possible involvement of glutamate receptor genes in the pathogenesis of schizophrenia, on the basis of association as well as linkage and postmortem studies previously reported. Replication of positive associations using different populations and the family-based study are necessary to confirm the results. Generation of gene-manipulated mice to represent endophenotypes of schizophrenia would be an alternative way to verify susceptibility genes. Some members of the glutamate receptor family may be promising targets for schizophrenia drugs. (C) 2003 Wiley-Liss, Inc.