Our research
We aimed to dissect the mechanisms of stress-related psychiatric disorders.
Re-phenotyping major depression
Current methods of clinical diagnosis for major depression are not sufficent and might not reflect the biological mechanisms behind. We combined in vivo Ca2+ imaging, automatic behavioural tracing and molecular sequencing to address this.
In collaboration with Prof. Mackenzie Mathis, EPFL
Neural circuits of anhedonia
Anhedonia, as a core symptom of major depression are not fully understood. We apply home-cage device FED3 to record reward seeking behaviours across time. We use viral tracing to identify brain regions that are involved. We aimed to manipulate these neural circuits to investigate anhedonia in major depression.
This project is funded by BBRF
Social valence in the extended- amygdala
As social interactions include both positive and negative aspects, an animal needs to properly evaluate different inputs from conspecifics to generate appropriate behavioural responses according to the cues. We will bring novel insights into the involvement of extended amygdala in social preference, and how interactions between the neuropeptide corticotropin releasing hormone (CRH) and dopamine (DA) systems shape the valence of social interaction under physiological and psychopathological conditions.
This project is funded by DFG under GRK2174
Stress comparison in the amygdala
Chronic stress is one of the key factors leading to major depression, however, we do not have a full picture of how stress affects different brain regions. We aimed to compare different stressors and their effects on neural activity, behaviours and gene expressions to identify the common ground of stress- related psychiatric disorders in the amygdala.
Rewiring after stress
Chronic stress might reshape the brain at meso- and micro scales. We aimed to compare different stressors and their effects on architectural changes and identify the mechanisms behind these changes.
In collaboration with Dr. Alba Vieites-Prado, CIMUS