Экспрессия генов глутаматных рецепторов в гиппокампе и лобной коре у крыс линии ГК с генетической кататонией

Abstract

The GC rat strain (the abbreviation of the words «genetic» and «catatonia») was obtained in the Institute of Cytology and Genetics of the SB RAS by breeding to enhance the passive-defensive freezing reaction in response to a weak stress stimulus. GC rats have a predisposition to catatonic reactions, as well as a number of behavioral and biochemical features corresponding to the homologous characteristics of patients with schizophrenia and depression. At the basis of the catatonic syndrome, as in schizophrenia, is believed to be the presence of a complex disturbance in functioning brain’s neurotransmitter systems, with special attention having been recently paid to glutamatergic system dysfunction, proposing the glutamate hypothesis of psychopathologies. Glutamate is the main excitatory mediator in the central nervous system and realize physiological effects through ionotropic (AMPA-, NMDA-, kainate) and metabotropic (mGlu) glutamate receptors. There are many studies indicating a change in the expression of glutamate receptor genes and the composition of their subunits in schizophrenia and bipolar disorders, as well as indicating the involvement of NMDA glutamate receptors in the manifestation of catatonic syndrome. In this regard, the aim of the work was to study the expression of the genes of glutamate system in the hippocampus and the frontal cortex of GC rats. Real-time PCR showed low expression of Grm3 gene encoding the metabotropic glutamate autoreceptor in the hippocampus of rats with genetic catatonia. The expression of Grin1, Grin2A, Grin2B, Gria1, Grm2, Slc17a6 in the frontal cortex and the hippocampus, as well as the Grm3 gene in the frontal cortex, did not differ from the control. Thus, the revealed low expression of mRNA of the Grm3 gene in the hippocampus can affect the neurotransmission of glutamate in this structure, and, among other things, contribute to an increase in nervous excitability in GC rats.