Functional modelling of the extended DISC1 pathway
Dysfunctions in synaptogenesis and synaptic transmission play a key role in the etiology of SCZ. However, hardly any of the components of the extended DISC1 pathway have been characterized in detail with respect to their role in synapse formation and function. The development of transgenic animals that model DISC1 dysfunction has been of outstanding importance in establishing DISC1 as a major behavioural and neuroanatomical modifier, A link of DISC1 suppression with disturbances in dopamine and glutamate metabolism has been demonstrated but information with other neurotransmitter systems is missing.
It is also unclear to what extent the well-established influence of DISC1 expression on cortical architecture and interneuron number relates to the solid behavioural changes.
Key objectives of this research team are therefore to
- Delineate signalling pathways functionally relevant at the synapse,
- Investigate the influence of DISC1 in animal models on neurotransmitters systems in the brain,
- Characterize the behavioural phenotype induced by DISC1 overexpression and
- To elucidate both the relation between the cortical architecture defects and PV cell number reduction to phenotypes.