Anhedonia at experimental models of chronic stress and its correction.

INTRODUCTION

Different types of chronic stress lead to neurotic and depressive disorders. Key symptoms of these disorders are anhedonia and correction of which will indicate the efficacy of proposed therapy. The aim of the paper is to investigate the influence of amide 2-hydroxy-N-naftalen-1-il-2-(2-oxo-1,2-dihidro-indole-3-iliden) and ethyl ether 4-[2-hydroxy-2-(2-oxo-1,2-dihidro-indole-3-iliden)-acetamin]-butyric acid on anhedonia after the experimental neurosis and chronic moderate stress in rats.

MATERIALS AND METHODS

It was studied the influence of therapeutic and preventive administration of substances 18 and E-38 in the dosage of 12mg/kg during chronic mild stress "conflict of afferent activation" during 30 days and depression-like behavior chronic mild stress that modeled 8 weeks. Results of investigation: Experimental neurosis caused decrease of number of comings to drinking-bowl, decrease of total number of drank sucrose and decrease of the percent of drank water with sugar in comparison with intact animals. Analogical but more significant changes were noticed during depression-like behavior. The use of amide 2-oxoindolin-3-glyoxylic acid based on neurosis counters effectively the development of anhedonia. Substance 18 increased the number of comings to drinking-bowl with sucrose and increased the amount of the number of drank water with sucrose in comparison with control pathology without correction. The substance possibly assists in use of solution with sucrose among water and does not compromise reference-preparation such as diazepam. The administration of ethyl ether of 2-oxoindolin-3-glyoxylic acid at chronic mild stress possibly increased the number of comings to the drinking-bowl and increased the number of drank sucrose in comparison with control pathology and it was more effective than imipramine and countered anhedonia.

CONCLUSIONS

It was indicated that during 30 day experimental neurosis and 8 week depression-like behavior cause the development of anhedonia. Therapeutic use of amide 2-hydroxy-N-naftalen-1-il-2-(2-oxo-1,2-dihidro-indole-3-iliden) and ethyl ether 4-[2-hydroxy-2-(2-oxo-1,2-dihidro-indole-3-iliden)-acetamin]-butyric acid corrected effectively anhedonia after experimental neurosis and chronic mild stress in rats.