Symposia

Programming human cognitive development and stress related disorders

There is good evidence that mental and physical health and alterations in neurodevelopment underlying variation in behaviour have their origins in prenatal and early postnatal life. Exposure to adverse environmental factors in early life is shown to affect developing brain areas and to be associated with changes in neuronal circuits that are involved in emotional processing, cognitive functioninig and modulating stress responses and. All studies of our symposium have a prospective design. We focus on the association between prenatal exposure to maternal stress and anxiety, maternal licorice consumption and famine – and offspring’s mental and physical health and behaviour in large cohort studies in UK, Finland, Australia and the Netherlands. The role of maternal and offspring hypothalamus-pituitary-adrenocortex (HPA) -axis function and the placenta as underlying mechanisms are discussed.

Chair: Bea Van den Bergh

Speakers:

• Viviette Glover
• Kati Räikkönen
• Anke van Eekelen
• Tessa Roseboom

Stress and stress hormones: processing and storage of emotional information

Relevant information is always accompanied by emotion. Social information and/or energy cues tend to be emotional. Stress facilitates the processing of important rather than non-significant information. Thereby, stress will interact with emotion, social information, and energy cues. The proposed symposium will present studies in humans that explore (i) how genetic differences in the glucocorticoid system affect emotional memory, (ii) whether stress will impact on the consolidation of socially relevant face identity and expression memory, (iii) how stress influences social threat processing, and (iv) how psychosocial stress modulates habitual behavior in an appetitive learning task.

Chair: Melly S. Oitzl

Speakers:

• Dominique de Quervain
• Hartmut Schächinger
• Karin Roelofs
• Oliver Wolf

Towards personalized medicine in stress related disease

Stress is a state of disturbed homeostasis following a threat by a real of imagined stressor. The stress response is composed of a manifold of adaptive reactions, including activation of the hypothalamic-pituitary-adrenal (HPA) axis. Most humans who experience trauma, acute or chronic stress, do not develop psychopathology. Only in some individuals which are vulnerable due to genetic factors or developmental influences stress-related disorders such as PTSD or depression will precipitate. This poses the questions 1. which specific genes are involved, 2. how do they interact with the environment and 3. can this knowledge be used to improve treatment.

Both Genome Wide Analysis (GWA) and the candidate gene approach have been employed to identify genetic factors. However, it is becoming clear that different gene-variants show specific interactions with environmental influences. A further complication is the clinical phenotype of psychiatric disorders which is often complex and diffuse. Despite these hurdles, several gene variants have been identified explaining in part individual disease course and treatment efficacy.

Chair: Erik Giltay

Speakers:

• Roel de Rijk
• Marcus Ising
• Jay Belsky
• Marieke Wichers

Looking into the stressed brain

Neuroimaging techniques have developed rapidly over the past years, providing increasingly sophisticated tools for the examination of brain function and structure in relation and reaction to stress. This technical development is paralleled by the introduction of novel neuroimaging paradigms designed to disentangle complex processes and interactions in the stressed brain.
In this symposium the speakers will present examples of this approach in the studies of stress regulation, the modulation of cognitive and emotional function by stress, and fear conditioning and extinction.

Chair: Nic van der Wee

Speakers:

• Jens Pruessner
• Anda van Stegeren
• Erno Hermans
• Christian Büchel

Novel translational research persectives on stress and depression

Chronic or traumatic stress is one of the best characterized environmental risk factors for affective disorders. While it is clear that genetic or epigenetic variations predispose certain individuals
to be more vulnerable to stress exposure, this complex gene-environment interaction is only poorly mimicked by many of the established animal models of depression. This symposium will therefore
highlight a number of new and translational strategies in modelling stress and depression. The speakers will illustrate how a paradigm shift in the recent years has led to novel approaches, including paradigms focusing on the interaction of genetic background with environmental challenges.

Chair: Thomas Steckler

Speakers:

• Jaap Koolhaas
• Igor Branchi
• Gregers Wegener
• Mathias Schmidt

From epigenetics to proteins: new approaches and insights in psychopathology

This session aims to connect past and current breakthroughs in stress research with exciting new developments in the emerging research areas of epigenetics and brain plasticity. Different approaches and new technologies will be presented which should enable us to identify novel pathophysiological mechanisms of stress-related mood disorders, as well as to evaluate potential novel treatments for these diseases.

Chair: Jos Prickaerts

Speakers:

• Hans Reul
• Moshe Szyf
• Chris Turck
• Herbert Covington

Consequences of chronic psychosocial stress: behaviour, neurons and immunology

Chronic stress is a burden of modern societies and is known to be a risk factor in numerous somatic and affective disorders, including inflammatory bowel disease (IBD), colonic carcinogenesis, chronic pain, anxiety- and depression-related diseases and systemic immunological dysfunctions. However, there are only a few clinically relevant animals models available to study the underlying mechnisms of chronic stress-induced diseases in detail. In this sympsium, leading scientists in the field will present detailed neuronal, behavioural, immunological and other systemic (mal-) adaptations as a result of chronic psychosocial stress in relevant rodent models, for example based on dominant-subdominant hierarchies Stefan Reber will start to present a recently established mouse model of chronic subordinate colony housing resulting in various neuroendocrine, immunological, and behavioural alterations. He will, futhermore show molecular and cellular mechanisms underlying chronic stress-induced adrenal insufficiency causally involved in immune alterations leading to acute colonic inflammation. Additive effects of early life stress and chronic stress in adulthood strongly affect these relevant behavioural and physiological parameters.
Carmen Sandi will continue on the consequences of exposure to chronic stress during infancy and puberty on the development of emotional alterations and abnormal social behaviour, as well as on the mechanisms that mediate these effects. She will present work implicating changes in gene expression (serotonergic pathways) in the prefrontal cortex and epigenetic mechanisms linked to these long-term effects. John Cryan will continue to elaborate on the impact of chronic stress and also early life stress on brain-gut axis communication. In particular the neural circuitry underlying such changes will be discussed and the impact of genetics and dietary factors will be highlighted

Chair: Inga Neumann

Speakers:

• Carmen Sandi
• Stefan Reber
• John Cryan

How the brain responds quickly to stress: Focus on corticosteroids

Stress hormones reach the brain shortly after stress exposure. Classically, it was thought that brain function is rapidly affected by monoamines, followed several hours later by corticosteroid hormones. However, exciting studies have now shown that corticosteroids also rapidly affect brain function.

First, Astrid Linthorst will show that after stress corticosteroid levels not only change quickly in the circulation, but also in limbic brain regions. Luke Johnson will then present EM data demonstrating corticosteroid receptors in the plasma membrane of limbic cells. Henk Karst will report that function of hippocampal and amygdalar neurons is rapidly changed by corticosterone. Finally, Jeffrey Tasker shows that in the hypothalamus too cells quickly respond to corticosterone, contributing to rapid feedback of the HPA-axis.

Chair: Marian Joels

Speakers:

• Astrid Linthorst
• Luke Johnson
• Henk Karst
• Jeffrey Tasker

Stress, inflammation and depression

Stress can activate the HPA axis and trigger inflammatory responses, both of which significantly contribute to the aetiology of depression and neurodegenerative diseases. In this symposium four experts will present and discuss their recent findings in 1) HPA axis and immune interaction in stress related disorders; 2) the relationship between stress and inflammation in the dysfunction of endothelial cells and the heart in depressed patients before and after treatment with SSRI’s or SNRI’s; 3) chronic stress and depression combination with chronic low grade inflammation to decrease neuronal repair by the tryptophan-kynurenine pathway and neurotrophins and 4) the mechanism of inflammation by which activating the HPA axis and suppressing neurotrophic system induces depressive and neurodegenerative changes.

Chair: Cai Song

Speakers:

• Ted Dinan
• Angelos Halaris
• Brian Leonard
• Cai Song