Expression of Glutamate Receptor Genes in the Hippocampus and Frontal Cortex in GC Rat Strain with Genetic Catatonia

The GC (genetic catatonia) rat strain was bred by selection aimed at enhancing the passive-defensive freezing response to a weak stressful stimulus. GC rats have a genetic predisposition to develop catatonic responses, as well as a number of behavioral and biochemical features corresponding to the homologous characteristics of patients with schizophrenia and depression. The catatonic syndrome, like schizophrenia, is believed to be based on a complex disturbance of the brain neurotransmitter systems. Since recently, special attention is being paid to the dysfunction of the glutamatergic system within the glutamate hypothesis of psychopathologies. Glutamate is the major excitatory neurotransmitter in the central nervous system; it mediates its physiological effects through ionotropic (AMPA-, NMDA-, kainate) and metabotropic (mGlu) glutamate receptors. Numerous studies indicate a change in the expression of glutamate receptor genes and the composition of receptor subunits in schizophrenia and bipolar disorders, as well as the involvement of NMDA glutamate receptors in the manifestation of the catatonic syndrome. In this regard, the aim of the work was to study the expression of glutamate system genes in the hippocampus and frontal cortex of GC rats. Real-time PCR showed low expression of the Grm3 gene (encoding a metabotropic glutamate autoreceptor) in the hippocampus of rats with genetic catatonia. The expression of Grin1, Grin2A, Grin2B, Gria1, Grm2 and Slc17a6 genes in the frontal cortex and hippocampus, as well as of the Grm3 gene in the frontal cortex, was indistinguishable from the control. Thus, the revealed low expression of Grm3 mRNA in the hippocampus may affect glutamate neurotransmission in this brain structure and, specifically, contribute to increased nervous excitability in GC rats.