Abstract

Introduction. Anxiety disorders are highly prevalent and are associated with high levels of morbidity and high great economic cost, These disorders affect up to 25% of population at some point in their lifetime. Anxiety can cause or aggravate many other diseases and diseases are more onerous in presence of anxiety.
Aim of the study. The general goal of the study was to establish new molecular targets implicated in the regulation of anxiety, because although effective treatments are available, they have a high abuse potential and serious adverse effects.
Methods. For this purpose, a model of innate anxiety based on exposure to cat odour was used. Male Wistar rats (Han/Kuo: WIST) as well as CCK2 receptor deficient mice and their wild-type littermates were exposed to cat odour cloth or clean cloth (control group). During and after cat odour exposure, the measures of the exploratory activity reflecting anxiety were assessed in  the animals. Thereafter, gene expression changes in the anxiety-related brain areas were studied as well using quantitative real-time PCR and cDNA Representational Difference Analysis.
Results and conclusions. Cat odour exposure induced several changes in the expression of the cholecystokinin and endogenous opioid systems. The biggest changes in gene expression were found in the temporal lobe, especially in the amygdala. The CCK2 receptor deficient mice showed a different gene expression profile and behavioural pattern compared to the wild-type littermates. It was established that a significant number of the genes previously unrelated to anxiety were differently expressed after cat odour exposure. Three of them were selected for further studies: Gamm1 gene, which is related to skin pigmentation; Wfs1 gene, which is linked to mood disorders and diabetes; and Lsamp, which is a gene responsible for development of the limbic system.