20-23 september 2017. Pécs - Hungary
Symposia
Recent advances in understanding of individual differences in stress resilience and vulnerability (Tamás Kozicz)
Recent advances in understanding of individual differences in stress resilience and vulnerability (Tamás Kozicz) 2017-09-23 - 10:00-12:00
Venue: Plenary Hall
Numerous factors make us react to stress differently. Mechanisms of individual differences in stress vulnerability vs. resilience suggests that there are brain structure and function specific effects of stress responsivity, which are influenced by the individual's prior experience shaping molecular, cellular and ultimately behavioral responses to stressful challenges.

MAIN ORGANIZER:

Tamás Kozicz MD, PhD (Chair)
Radboud University Medical Centre, Nijmegen, The Netherlands

 

SPEAKERS:

10:00 – 10:25 Carmen Sandi
Brain Mind Institute, Ecole Polytechnique Federale de Lausanne, Switzerland
"The role of brain bioenergetics on the effects of stress and anxiety in brain function and coping behaviors"

10:25 – 10:50 Jan Deussing
Max Planck Institute of Psychiatry, Munich, Germany
"Towards genetic factors and neuronal circuits that shape emotional behaviors and stress vulnerability" 

10:50 – 11:10 Anikó Kőrösi
Structural and Functional Plasticity of the Nervous System, Swammerdam Institute for Life Sciences,
University of Amsterdam, The Netherlands
"Programming of cognitive functions by early-life stress: a role for nutrition and potential for intervention"

11:10 – 11:25 Balázs Gaszner
Department of Anatomy, Medical School, University of Pecs, Hungary 
„The three hit concept of depression. What does maternal deprivation and superimposed chronic mild stress do in PACAP mutant mice?"

11:25 – 11:40 Teun Klein-Gunnewiek
Department of Anatomy, Radboud University Medical Centre
Nijmegen, The Netherlands
"Human iNeuron model of mood disorders in patients with mitochondrial disorder"

11:40 – 12:00 Discussion

 

SUMMARY

Stress is everywhere. But how does the brain process stress, and most important what conveys individual differences in stress responsivity that leave some of us vulnerable and others resilient to stress-related psychopathology? The speakers of this symposium will take the audience through observations on brain region- and cell type-specific effects of stress signaling that are influenced by the individual's prior experience and that shape molecular, cellular and ultimately behavioral responses to stressful challenges. First, Dr. Sandi will discuss her work linking individual differences in mitochondrial function –as observed for example in individuals differing in anxiety traits- in specific brain areas with behavioral vulnerability to stress. Her talk will focus on the behavioral impact of brain bioenergetics and on the identification of mediating mechanisms implicating specific gene pathways. Dr. Deussing will interrogate the interactions between potential genetic risk factors and stress as an environmental factor focusing on specific neuronal circuits. He will show that emotional behavior and individual stress resilience vs. vulnerability strongly depend on the temporal and spatial involvement of a given neuronal circuit as well as previous stress experiences. Dr. Korosi states that early-life stress is associated with cognitive decline in adulthood. She will show evidence on the possible role of nutrition and highlight the relevance of nutrients in the programming effects of early-life stress and point to early dietary intervention as a novel non-invasive target to prevent the early-life stress induced deficiencies. Dr. Gaszner will show functional morphological data suggesting that the dysregulation of the pituitary-adenylate cyclase-activating polypeptide system modulates the ability of mice to cope with stress within the framework of the three-hit concept of stress-related psychopathology. Lastly Klein-Gunnewiek will present data on forebrain specific human neuronal progenitor cells (iNeuron) derived from induced pluripotent stem (iPS) cell lines from depressed mitochondrial patients. He will argue that the increased vulnerability of patients with mitochondrial disorders to depression is underpinned by altered neuronal development and synapse-related deficits.