Schmidt, Manuela, Dr.
- Since 2012: Emmy Noether Group Leader
- 2007-2012: Postdoc with Ardem Patapoutian, The Scripps Research Institute, La Jolla, California, USA
- 2002-2006: PhD, Neurosciences, International Max Planck School Neurosciences, Laboratory of Stephan Sigrist, ENI-G, Goettingen, Germany
- 2001-2002: Master, Neurosciences, International Max Planck School Neurosciences, Goettingen, Germany
- 1997-2002: Diploma, Biology, University of Wuerzburg, Germany
What are the specific dynamic changes that occur at the molecular, cellular and network levels in nociceptors during acute and chronic pain?
How are these changes mirrored in pain-related regions of the central nervous system?
Homepage Department/Research Group
Selected Recent Publications
Major Research Interests
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 somatosensory signaling networks 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:
- Rouwette T, Avenali L, Sondermann J, Narayanan P, Gomez-Varela D, Schmidt M. (2015) Modulation of nociceptive ion channels and receptors via protein-protein interactions - implications for pain relief. Channels (Austin). 2015 Jul 4;9(4):175-85. doi: 10.1080/19336950.2015.1051270. Epub 2015 Jun 3.
- Coste B, Murthy SE, Marthur J, Schmidt M, Mechioukhi Y, Delmas P, Patapoutian A. (2015) Piezo1 ion channels pore properties are dictated by C-terminal region. Nature Communications 6; doi:10.1038/ncomms8223
- Avenali L, Narayanan P, Rouwette T, Cervellini I, Sereda M, Gomez-Varela D, Schmidt M. (2014). Annexin A2 Regulates TRPA1-Dependent Nociception. J Neurosci. 34(44):14506-16. doi: 10.1523/JNEUROSCI.1801-14.
- Dubin AE, Schmidt M, Mathur J, Petrus MJ, Xiao B, Coste B, Patapoutian A (2012) Inflammatory signals enhance piezo2-mediated mechanosensitive currents. Cell Rep. Sep 27;2(3):511-7
- Gˇmez-Varela D, Schmidt M, Schoellerman J, Peters EC, Berg DK (2012) PMCA2 via PSD-95 Controls Calcium Signaling by ?7-Containing Nicotinic Acetylcholine Receptors on aspiny Interneurons. J Neurosci. 16;32(20):6894-905
- Coste B, Xiao B, Santos JS, Syeda R, Grandl J, Spencer KS, Kim SE, Schmidt M, Mathur J, Dubin AE, Montal M, Patapoutian A (2012) Piezo proteins are pore-forming subunits of mechanically activated channels. Nature 19;483(7388):176-81
- Coste B, Mathur J, Schmidt M, Earley TJ, Ranade S, Petrus MJ, Dubin AE, Patapoutian A (2010) Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels Science, 330: 55-60
- Schmidt M, Dubin AE, Petrus MJ, Earley TJ, Patapoutian A (2009) Nociceptive signals induce trafficking of TRPA1 to the plasma membrane. Neuron 64(4):498-509