Expression of catecholaminergic genes in the midbrain and prepulse inhibition in rats with a genetic catatonia

Abstract

The GC rat strain (from the words “genetic” and “catatonia”) was created by selection for predisposition to passive-defensive reaction of catatonic freezing in response to stressing stimuli. Rats of the GC strain have previously demonstrated a number of biochemical and behavioral properties similar to those of patients with schizophrenia and depression. Prepulse inhibition (PPI) is widely explored as an important indicator, a decrease of which may be indicative of psychopathology, including schizophrenia. It has been established that the brain noradrenergic system influences the manifestation of PPI, in particular through the activation of central alpha-adrenoreceptors. Also known is the association between PPI and expression of catechol-O-methyltransferase. This study focuses on the reaction of prepulse inhibition in rats of the inbred GC strain, being considered as a hypothetical model of schizophrenia, as well as on the relation of prepulse inhibition to mRNA expression of tyrosine hydroxylase, catechol-O-methyltransferase, alpha1A- and alpha2Aadrenergic receptors in the midbrain of GC rats. For the first time, a decrease of PPI in GC rats compared with WAG rats was shown, both with a prepulse power of 75 dB and at 85 dB, which may indicate a violation of filtration of sensorimotor information into the central nervous system in GC rats. Real-time PCR showed a decrease in mRNA level of Adra1A in intact rats with genetic catatonia when compared to control WAG rats. There was observed no correlation between the expression of mRNA of the Adra1A, Adra2A, Th, and Comt genes in the midbrain and the PPI reaction in GC rats. The reduction of prepulse inhibition in GC rats indicates functional similarity of this genetic model of schizophrenic psychopathology with a prototype.