Marshall Devor (Neuroscience)

Marshall Devor (Neuroscience)

Devor (Neuroscience)
Department of Cell & Developmental Biology Institute of Life Sciences
Faculty of Mathematic and Natural Sciences,
Hebrew University of Jerusalem, Givat Ram, Jerusalem 91904
Phone: +972 2-658-5085 , Fax: +972 2-658-6027


Prof. Devor is the Alpert Professor of Pain Research at the Hebrew University of Jerusalem (HUJI). He was born in Toronto, Canada in 1949. His AB and PhD degrees were from Princeton University (1970) and MIT (1975). He was a postdoctoral fellow with the pain research pioneer Prof. P.D. Wall at University College London and later at HUJI. He joined the HUJI faculty as Research Associate in 1977 and rose to the rank of Professor in 1988. He served as Department Chairman (3 terms) and in a number of other University, national and international roles. He has contributed considerably to the understanding of the physiological basis of neuropathic pain and more recently to mechanisms involved in loss of consciousness and pain-free surgery. He is author of ~300 publications (H index = 69).


I am most proud of a series of innovative scientific contributions that opened new research avenues and in which my research papers were the first, or among the first, in the literature. These include: 
  • Among the first research on collateral sprouting in the skin following nerve injury (rats & humans).
  • Established ectopic discharge in nerve end neuromas as a fundamental factor in neuropathic pain.
  • Discovery of "sympathetic-sensory coupling" as a factor in neuropathic pain, and its association with sympathetic sprouting in the nerve end and the dorsal root ganglion (DRG).
  • Establishment of the first animal model of neuropathic pain, the "neuroma model", still widely used.
  • First demonstration of ephaptic crosstalk at nerve injury sites, previously only a medical speculation.
  • Discovery of neuroplastic reorganization of somatosensory maps in the spinal dorsal horn and cortex following peripheral nerve injury. This work was subsequently extended to primates and humans.
  • Discovered role of Na+ channel accumulation in axons to hyperexcitability and neuropathic pain.
  • Demonstrated that corticosteroids and anticonvulsants suppress ectopia and hence neuropathic pain.
  • Discovered neuropathic hyperexcitability in DRG neurons & role of sub-threshold oscillations in ectopia.
  • Discovery of non-ephaptic/non-synaptic crosstalk among injured afferent axons and DRG somata.
  • Developed the "Ignition Hypothesis" of paroxysmal pain in Trigeminal Neuralgia.
  • Novel mechanism and treatment for osteoarthritic pain based intrinsic innervation & root canal analogy
  • Discovery that susceptibility to neuropathic pain is heritable; among the founders of Pain Genetics.
  • Identification of Cacng2 (stargazin) as a susceptibility gene for neuropathic pain (animals and man).
  • First use of correlational analysis for defining fundamental pain "types", and gene expression changes.
  • Use of selection-line strains to discover pain-relevant genes.
  • Discovered the brainstem MPTA, a key node in the network sub-serving anesthetic state transitions.

Sample of recent research publications:

  1. Anesthetic loss of consciousness induced by chemogenetic excitation of mesopontine effector neurons.
    Baron M, Vaso K, Avigdor T, Charit Y, Minert A, Devor M.
    Exp Neurol. 2022 Jul 9;357:114169. doi: 10.1016/j.expneurol.2022.114169. Online ahead of print.PMID: 35817130

  2. Resurgent neuropathic discharge: an obstacle to the therapeutic use of neuroma resection?
    Tal M, Minert A, Devor M.
    Pain. 2022 May 28. doi: 10.1097/j.pain.0000000000002704. Online ahead of print.PMID: 35639421

  3. Might pain be experienced in the brainstem rather than in the cerebral cortex?
    Baron M, Devor M.
    Behav Brain Res. 2022 Jun 3;427:113861. doi: 10.1016/j.bbr.2022.113861. Epub 2022 Mar 26.PMID: 35346731

  4. Searching in the wrong place: Might consciousness reside in the brainstem?
    Devor M, Koukoui M, Baron M.
    Behav Brain Sci. 2022 Mar 23;45:e46. doi: 10.1017/S0140525X21001928.PMID: 35319425

  5. Anesthesia in mice activates discrete populations of neurons throughout the brain.
    Yatziv SL, Yudco O, Vaso K, Mizrahi A, Devor M.
    J Neurosci Res. 2021 Dec;99(12):3284-3305. doi: 10.1002/jnr.24950. Epub 2021 Sep 12.PMID: 34510528

  6. A nodal point for brain-state transitions: the mesopontine tegmental anesthesia area (MPTA) in mice.
    Yatziv SL, Strumza N, Minert A, Baron M, Devor M.
    Exp Brain Res. 2021 Nov;239(11):3255-3266. doi: 10.1007/s00221-021-06204-7. Epub 2021 Aug 30.PMID: 34459944

  7. Paradoxical anesthesia: Sleep-like EEG during anesthesia induced by mesopontine microinjection of GABAergic agents.
    Avigdor T, Minert A, Baron M, Devor M.
    Exp Neurol. 2021 Sep;343:113760. doi: 10.1016/j.expneurol.2021.113760. Epub 2021 May 15.PMID: 34000248

  8. Patterns of neural activity in the mouse brain: Wakefulness vs. General anesthesia.
    Yatziv SL, Yudco O, Dickmann S, Devor M.
    Neurosci Lett. 2020 Sep 14;735:135212. doi: 10.1016/j.neulet.2020.135212. Epub 2020 Jun 25.PMID: 32593772

  9. Individual Mesopontine Neurons Implicated in Anesthetic Loss-of-consciousness Employ Separate Ascending Pathways to the Cerebral Cortex.
    Lellouche Y, Minert A, Schreiber C, Aroch I, Vaso K, Fishman Y, Devor M.
    Neuroscience. 2020 Apr 15;432:188-204. doi: 10.1016/j.neuroscience.2020.02.022. Epub 2020 Feb 26.PMID: 32109530

  10. Reduced Sensitivity to Anesthetic Agents upon Lesioning the Mesopontine Tegmental Anesthesia Area in Rats Depends on Anesthetic Type.
    Minert A, Baron M, Devor M.
    Anesthesiology. 2020 Mar;132(3):535-550. doi: 10.1097/ALN.0000000000003087.PMID: 31850942