The Scherrer Laboratory at Stanford University School of Medicine investigates the identity of the sensory (A), spinal (B), and brain (C) neurons that constitute pain neural circuits, and the molecular mechanisms that control neural activity and behavior associated with pain perception and analgesia.

Dr. Scherrer earned his PhD in cellular and molecular biology from the University of Strasbourg, France. He completed postdoctoral training at the University of California, San Francisco, and at Columbia University. He joined the faculty at the Stanford University School of Medicine in 2012. In addition to a Rita Allen Foundation Scholar award, he has received an International Association for the Study of Pain Postdoctoral Fellowship, a National Institutes of Health/National Institute on Drug Abuse K99R00 Pathway to Independence Award, a Department of Defense Neurosensory Research Award and an International Narcotics Research Conference Young Investigator Award.

The members of the Scherrer laboratory want to understand how neural circuits are functionally organized to encode qualitatively and quantitatively distinct pain signals, and to allow discrimination of pain from other somatosensory experiences such as touch or itch. Their ultimate goal is to identify the changes in this organization that underlie pathologic chronic pain and to discover new molecular targets to treat this disease. One of their approaches is to gain understanding of how our endogenous opioid system functions. Opioid receptors and peptides composing this system modulate pain threshold and underlie the effect of the oldest, but still most effective, pain killers—namely, opium poppy-extracted morphine and its derivatives. The Scherrer laboratory seeks to establish the mechanisms by which opioids generate analgesia and detrimental side effects (e.g., tolerance, addiction, hyperalgesia) to develop more efficient and safer analgesic treatments for managing pathologic pain. To reach this goal, they combine a variety of experimental approaches, including mouse genetics, molecular biology, neuroanatomy, electrophysiology, optogenetics, in vivo calcium imaging and behavior.

Sessions at Neurovations Events

2017 Napa Pain Conference

Awards

  • International Trainee Fellowship funded by the Scan|Design Foundation BY INGER & JENS BRUUN, International Association for the Study of Pain (2009)
  • K99/R00 Pathway to Independence Award, National Institutes of Health – National Institute on Drug Abuse (2011)
  • Rita Allen Foundation Scholar, Rita Allen Foundation – American Pain Society (2014)
  • Neurosensory Research Award, Department of Defense (2014)

Select Publications

  • A Brainstem-Spinal Cord Inhibitory Circuit for Mechanical Pain Modulation by GABA and Enkephalins. Neuron François, A., Low, S. A., Sypek, E. I., Christensen, A. J., Sotoudeh, C., Beier, K. T., Ramakrishnan, C., Ritola, K. D., Sharif-Naeini, R., Deisseroth, K., Delp, S. L., Malenka, R. C., Luo, L., Hantman, A. W., Scherrer, G.2017; 93 (4): 822-839 e6
  • Loss of mu opioid receptor signaling in nociceptors, but not microglia, abrogates morphine tolerance without disrupting analgesia NATURE MEDICINE Corder, G., Tawfik, V. L., Wang, D., Sypek, E. I., Low, S. A., Dickinson, J. R., Sotoudeh, C., Clark, J. D., Barres, B. A., Bohlen, C. J., Scherrer, G.2017; 23 (2): 164-173
  • In Vivo Interrogation of Spinal Mechanosensory Circuits. Cell reports Christensen, A. J., Iyer, S. M., François, A., Vyas, S., Ramakrishnan, C., Vesuna, S., Deisseroth, K., Scherrer, G., Delp, S. L.2016; 17 (6): 1699-1710
  • Structure-based discovery of opioid analgesics with reduced side effects NATURE Manglik, A., Lin, H., Aryal, D. K., McCorvy, J. D., Dengler, D., Corder, G., Levit, A., Kling, R. C., Bernat, V., Huebner, H., Huang, X., Sassano, M. F., Giguere, P. M., Loeber, S., Duan, D., Scherrer, G., Kobilka, B. K., Gmeiner, P., Roth, B. L., Shoichet, B. K.2016; 537 (7619): 185-?
  • Enhanced dendritic integration by ih reduction in the anterior cingulate cortex increases nociception. Neuron Dickinson, J. R., Scherrer, G.2015; 86 (1): 4-6
  • GINIP, a G(alpha i)-Interacting Protein, Functions as a Key Modulator of Peripheral GABA(B) Receptor-Mediated AnalgesiaNEURON Gaillard, S., Lo Re, L., Mantilleri, A., Hepp, R., Urien, L., Malapert, P., Alonso, S., Deage, M., Kambrun, C., Landry, M., Low, S. A., Alloui, A., Lambolez, B., Scherrer, G., Le Feuvre, Y., Bourinet, E., Moqrich, A.2014; 84 (1): 123-136