Henrike Hartung received her M.Sc. in Neuroscience (2005) and D.Phil. (2009) from the University of Oxford, UK. Her work on the role of the gaseous neuromodulator nitric oxide in the nucleus accumbens, whose dysfunction has been associated with mental illness, laid the ground for her continuing interest in the circuitry and associated transmitter systems underlying psychiatric disorders. During her first post doc in Prof. Trevor Sharp’s lab at the Department of Pharmacology, University of Oxford, UK, she investigated the effect of deep-brain stimulation (DBS) as used for the treatment of Parkinson’s disease on the activity of the serotonergic system. DBS predominantly inhibited serotonergic neurons and decreased extracellular 5-HT levels in the forebrain, which may underlie psychiatric side effects of this treatment, such as depression.
Intrigued by the evidence that certain risk factors for mental disorders can arise already before, during or soon after birth made her focus on the developing brain. In 2012 she moved to Prof. Ileana L. Hanganu-Opatz’s lab at the University Medical Center Hamburg-Eppendorf, Germany. Using mouse models of combined genetic and environmental risk factors of schizophrenia, she found that functional communication between brain regions underlying cognition is already impaired during neonatal development long before deficits in cognitive behaviour emerge. Her current interests continue this line of research. In 2015 she moved to Prof. Kai Kaila’s lab at the Department of Biosciences and Neuroscience Center, University of Helsinki, Finland where she investigates the risk factors related to complicated birth and, in particular, the effects of birth-associated fetal surge of the stress hormone arginine vasopressin on the development of networks underlying emotional behavior.
Brief description of research project
Psychiatric disorders including depressive and anxiety disorders are very common and posit the largest contributor to chronic conditions in Europe. Based on strong evidence that early adverse life events predispose an individual to develop mental disorders, there is an increasing consensus that they have a developmental origin. These risk factors include obstetric complications like hypoxia (low oxygen) associated with birth asphyxia. Insights into the mechanisms underlying increased susceptibility to disease come from studies in animal models that have found profound damage to the 5-hydroxytryptamine (5-HT, serotonin) system after neonatal asphyxia. Dysfunction of the 5-HT system has long been implicated in psychiatric disorders including depression, and recent evidence shows that a disordered 5-HT system during neonatal development impairs adult emotional behavior. The current research project aims at elucidating in an animal model whether neonatal asphyxia permanently alters the function of the developing 5-HT system; and whether these effects are mediated by stress hormones and, in particular, arginine vasopressin which is released during neonatal asphyxia. The results will provide novel insights into the ontogenetic background of psychiatric disorders and will help to design novel therapeutic strategies.