TIGEM’s Behavioral Core has three principal objectives. It aims to identify abnormal behaviors in animal models that may be associated with gene deletions or mutations pertaining to our human genetic diseases of interest. Upon finding such information, the Core tests whether and to which extent novel pharmacological or gene therapy techniques can be used to rescue these behavioral alterations. Last but not least, the Core organizes novel behavioural tasks and procedures to study rodent behavior in mice, rats, hamsters.
The Core combines basic knowledge of the biological processes underlying animal behavior with systematic use of the whole battery of behavioral tests available for rodents to date.
In support of its research, the Behavioral Core is equipped with more than 30 different behavioral task tools (i.e. activity cage, elevated plus-maze, hot-plate, water maze, cross-maze, grip-strength meter, passive and active avoidance apparatus) for mice, rats and hamsters, which allow it to test basic sensory-motor functions, learning and memory processes and emotional behaviors. The Core personnel helps and assists researchers in the planning, execution, data analysis, data interpretation, results dissemination, and application for grant funding for all behavioral and behavioral-pharmacogenetic experiments. Since its establishment in September 2007, the Core behavioral group has established eleven internal collaborations that have led to an accumulation of experience specific to the behavioral phenotyping of many different genetic animal models of human genetic diseases.
The Behavioral Core has worked to identify behavioral alterations in animal models of lysosomal storage disorders, in particular in those of mucopolysaccharidoses. Mucopolysaccharidoses are a group of monogenic, rare, incurable disorders affecting children. Some lead to progressive bone and articular defects (i.e. MPSVI), some cause neurodegeneration (i.e. MPS-III and MPS-II) and others generate both types of phenotypes (i.e. MSD). In the past years we have identified some specific behavioral alterations in each of these animals models, which we consider helpful parameters to test the efficacy and side effects of novel therapeutic strategies in vivo.
Finally, we are combining our expertise of lysosomal storage disorders with that of neuropsychopharmacology of learning and memory to identify early neurochemical dysfunction, which leads to the neurobehavioral phenotype in MPS animal’ models. These studies will add important information and help to explain the neurochemical changes that occur in MPS and affect the central nervous system. This may give new insights into the diseases mechanisms that originate as lysosomal storage disorders and lead to neurodegeneration.