The perception of and appropriate reaction to external and internal stimuli is critical for survival. In vertebrates, chemical, mechanical (from pleasant touch to painful contact) and thermal stimuli are detected by specialized somatic sensory neurons which transfer these signals via the spinal cord to the brain. An important subset of these neurons, so-called nociceptors, senses noxious stimuli. Consequently, their activation mediates nociception and leads to the sensation of pain.
Pain is the single most common symptom for which patients seek medical assistance. While acute pain has served as a protective mechanism throughout evolution to guard the body against injury, pain can also become chronic and highly debilitating. Unfortunately, chronic pain imposes substantial challenges to medical practice: current therapies can be effective for short-term treatment however many do not provide sufficient relief to chronic conditions or cause strong side-effects. Therefore, a deeper understanding of the molecular mechanisms underlying both, acute and chronic pain is crucially needed.
Our research focuses on the comparative and quantitative analysis of signaling complexes in established mouse models of acute and chronic pain. To this purpose our lab employs interactomics, genetic profiling, calcium-imaging, electrophysiology, neuronal tracing and mouse behavioral studies in order to address key questions:
1. What are the specific dynamic changes that occur at the molecular, cellular and network levels in nociceptors during acute and chronic pain?
2. How are these changes mirrored in pain-related regions of the central nervous system?
The identification of changes in signaling complexes which are specific to certain pain states should enable us to selectively modulate the respective complexes in vivo while leaving key physiological functions intact.