Altered glutamate receptor and corticoliberin gene expression in brain regions related to hedonic behavior in rats

Abstract

Present experiments in rats were aimed to verify the hypothesis that glutamatergic neurotransmission and stress hormones play a role in impairment of hedonic behavior, a sign of depression-like state. On the basis of individual variability in sucrose preference, test rats were divided into anhedonic and hedonic groups. Anhedonic animals showed higher basal concentrations of adrenocorticotropin and corticosterone but reduced hormonal responses during novelty stress compared to hedonic animals. Acute administration of citalopram (10 mg/kg ip) induced similar effects in both groups. Corticotropin-releasing hormone (CRH) mRNA levels in hypothalamic paraventricular nucleus (PVN) were higher in anhedonic rats. Oxytocin (OT) and vasopressin gene expression in the PVN and proopiomelanocortin (POMC) expression in the anterior pituitary failed to show any significant differences. Gene expression of NR1 receptor subunit of N-methyl- d-aspartate (NMDA) glutamate receptor in the ventral tegmental area (VTA) was found to be lower in anhedonic rats. In the nucleus accumbens (NAc) and the hippocampus of anhedonic animals, higher mRNA levels of NR2A subunit compared to those of hedonic rats were detected. Thus, low sucrose preference is associated with altered HPA axis activity, NMDA receptor subunits and CRH gene expression in selected brain regions. These mechanisms may operate in the disposition to develop hedonic deficit in some mental disorders.