Behavioural Neuroscience

The Behavioural Neuroscience Team investigates the molecular and genetic basis of behavioural and brain dysfunctions that are relevant for human neuropsychiatric disorders using the mouse as mammalian animal model. In this context we are particularly, but not exclusively, interested in neurodegenerative diseases and their genetic predisposing factors. 

Phenotypes are influenced by genetic predisposition, developmental processes and environmental factors. Therefore we subject genetically modified mouse lines that are presumed models for neuropsychiatric diseases to comprehensive behavioural and neurohistological phenotyping under baseline, different challenge or environmental conditions, to discover disease-related phenotypes. With this approach we generate new, or test known hypotheses of disease mechanisms in relevant mouse models, with the aim to indicate new avenues for therapeutic interventions and drug development. If appropriate, this analysis can be complemented by other comprehensive phenotyping methods in collaboration with our colleagues of the German Mouse Clinic (http://www.mouseclinic.de), in which we run the Behavioural Screen. 

Figure 1

Our behavioural test repertoire assesses motor, sensorimotor, emotional and cognitive phenotypes (see Fig. 1). In combination with these, pharmacological challenges can be applied if appropriate. The strategy for the brain analysis is determined by careful consideration of the phenotyping results in combination with all available information about the gene and the disease that are being studied (see Fig. 2). 

Figure 2

We assess neurohistological phenotypes known to be associated with schizophrenia, autism, anxiety, mood, intellectual disability and neurodegenerative disorders. We have established a methodology and a marker panel to detect alterations in different neuron populations, neurogenesis, neuroinflammation, neuronal cell morphology, synaptic protein expression, excitatory/inhibitory balance and brain region volumes (see Fig. 3).

Figure 3

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