Adverse early-life events predispose individuals to neuropsychiatric disorders. These early-life risk-factors include social stress by parental maltreatment, neglect or abuse but also birth-related complications. They have in common that they activate the stress axis of the body and trigger release of stress hormones during critical periods of brain development.
We aim to reveal how this postnatal surge in stress hormones affects the ongoing functional development of the serotonergic and dopaminergic system, whose malfunction has long been implicated in mental illness. Moreover, we study long-range interactions after early-life stress within networks regulating emotional behaviour and reactivity such as medial prefrontal cortex, hippocampus and amygdala. We posit that their altered maturation might underlie increased vulnerability to disease later on in life.
Our experimental approach includes in vivo electrophysiological recording techniques in combination with pharmacological manipulations and anatomical studies in rodent models.
Our research efforts have the goal to contribute further insights into the causes and mechanisms that underlie increased susceptibility to neuropsychiatric disorders. Such knowledge is crucial for the development of new treatment strategies that aim at disease prevention.