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Startseite > Forschung > Drittmittelprojekte / funded projects > SFB1158

SFB1158   ( englisch, Flagge )

https://www.sfb1158.de/
SFB 1158: From nociception to chronic pain: Structure-function properties of neural pathways and their reorganization

 

What underlies the ‘Dr. Jekyll and Mr. Hyde’ nature of this key physiological function that has protected the animal kingdom from harm throughout evolution?
Why does pain convert into a disorder by becoming chronic?
And importantly, can we prevent, treat or revert these changes?

These questions are at the heart of the new Heidelberg Pain Consortium. Established by the German Research Foundation at Heidelberg University in July 2015, this centre comprises nineteen multidisciplinary projects and several associated research endeavours that span diverse, top-class clinical and basic research institutes in the twin cities of Heidelberg and Mannheim.

A key task is to understand structure-function relations that determine sensory, emotional and cognitive processes and how these functionally integrate to form a system which underlies the highly subjective experience of acute pain. A further task is to study these in the context of chronic pain, which may involve more complex networks, comprising more ‘nodes’ and a higher degree of associations, given especially, potential, complex interactions with pathways governing emotional, motivational and cognitive processes that are also involved in psychopathological disorders, such as depression, addiction and anxiety.

To tackle these goals, a highly trans-disciplinary configuration, merging expertise in classical pain research with knowledge on other pathways, disorders and methodologies, is required. Indeed, this matches the conceptual as well as the technological repertoire of scientists working together in Heidelberg and Mannheim.

Research Area A consists of projects addressing key questions on the structure, function and specificity of distinct parts of the sensory afferent-spinal cord circuitry and the identification of genetic and epigenetic mechanisms which mediate specificity as well as structural and functional plasticity.