ABSTRACT
Receptor-like tyrosine kinase IRR (the insulin receptor-related receptor) can be activated by extra- cellular alkaline media. IRR is found in organs that come in contact with liquids of extremal pH, and also in specific cells of the nervous systems where its function is not known. In this study, we analyzed the phenotype of IRR knockout mice in a series of behavioral tests. In control experi- ments, null-mutation littermate mice were analyzed. In the "Social interaction" test, the knockout animals showed a reduced number of social contacts. No statistically significant differences in im- mobility time were revealed in the "Forced swim" test, yet the number of animals that showed pro- longed immobility time, was higher in the group of knockout mice. In the "Resident-intruder" test, wild-type mice demonstrated their typical aggressive behavior whereas 7 out of 16 knockout animals stayed inert and, in contrast, attacked by the intruder. The obtained data suggest that the IRR gene inactivation results in disturbances of the aggressive-defensive behavior typical of the parental mouse strain.
Subject(s)
Dominance-Subordination , Gene Deletion , Immobility Response, Tonic , Mice, Knockout/genetics , Receptor, Insulin/genetics , Aggression , Animals , Breeding , Female , Founder Effect , Grooming/physiology , Heterozygote , Homozygote , Hydrogen-Ion Concentration , Male , Mice , Mice, Inbred C57BL , Mice, Knockout/psychology , Phenotype , Receptor, Insulin/deficiencyABSTRACT
In this study, we found the sixth site of alternative splicing (SS6) of neurexin 1a from the rat brain. This site is located between the fifth LNS and the third EGF-like domains. The insertion in the SS6 site corresponds to the 9-residue peptide VALMKADLQ, which is conserved among animals. We demonstrated that the SS6 insertion regulates tissue-specific expression of neurexin 1α.
