ABSTRACT
We studied the effect of the organoselenium compound 2,6-dipyridinium-9-selenium-bicyclo[ 3,3,1]nonan dibromide (974zh) on the severity of pathological changes in the organs of experimental animals immunized with live tularemia and brucellosis vaccines. It was found that 974zh reduced reactogenicity of vaccines for experimental animals. Our findings indicate the prospects for further studies of the effects of 974zh on the functional state of experimental animals.
Subject(s)
Bacterial Vaccines/immunology , Brucellosis/immunology , Organoselenium Compounds/pharmacology , Synthetic Drugs/pharmacology , Tularemia/immunology , Animals , Magnetic Resonance Spectroscopy , MiceABSTRACT
Calsyntenin-2 (Clstn2) is the synaptic protein that belongs to the super family of cadherins, playing an important role in learning and memory. We recently reported that Clstn2 knockout mice (Clstn2-KO) have a deficit of GABAergic interneurons coupled with hyperactivity and deficient spatial memory. Given, that impaired functioning of GABA receptors is linked to several psychopathologies, including anxiety and autism, we sought to further characterize Clstn2-KO mice with respect to emotional and social behavior. Clstn2-KO males and females were tested in the elevated plus-maze (EPM), open field (OF), forced swim test, social affiliation and recognition test, social transmission of food preference (STFP), dyadic social interactions and marble burying test. Clstn2-KO mice demonstrated high exploration and hyperactivity in the dimly lit EPM that affect anxiety parameters. In contrast, in a more adverse situation in the OF have increased emotionality in Clstn2-KO males, not females. Assessment of hyperactivity for prolong period in the OF showed that Clstn2-KO animals were able to decline their hyperactivity, but their ambulation still remained higher than in WT littermates. Additionally, Clstn2-KO mice expressed stereotyped behavior. Strikingly, analysis of social behavior identified deficient social motivation and social recognition only in Clstn2-KO males, but not in females. Further analysis of social communication in the STFP and direct observation of agonistic interactions confirmed the reduced social behavior in Clstn2-KO males. Altogether, current results showed Clstn2 gene and sex interactions on socio-emotional performance in mice, suggesting a possible role of calsyntenin2 in psychopathological mechanisms of autism.