Professor Marshall Devor
born: Jan. 8, 1949 (Toronto, Canada)
Department for Cell and Animal Biology
Institute of Life Sciences, Hebrew University of Jerusalem
Jerusalem 91904, Israel
Tel. +972 2 6585085
Fax: +972 2 6586027
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. Lu J, Sherman D, Devor M, Saper CB. A putative flip-flop switch for control of REM sleep. Nature. 441 (2006) 589-594. Times Cited: 665 [This paper lays out the flip-flop concept of sleep regulation]
2. Devor, M. Sodium channels and mechanisms of neuropathic pain. Journal of Pain, S1 (2006) S3-S12 Times Cited: 253 [This paper summarises in a digestible form my research on the subject, beginning in 1989, a time a relationship between Na+ channels and neuropathic pain was not yet on the map]
3. Devor, M. Pathophysiology of Nerve Injury in: Handbook of Clinical Neurology, 3rd series, vol. 81, Pain. F. Cervero and T.S. Jensen eds. Elsevier pp. 261-276 (2006). [A famous series in Clinical Neurology]
4. Persson A-K, Gebauer M, Jordan S, Metz-Weidmann C, Schulte AM, Schneider H-C, Thun J, Xu X-J, Wiesenfeld-Hallin Z, Darvasi A, Fried K, Devor M. Correlational analysis for identifying genes whose regulation contributes to chronic neuropathic pain. Molecular Pain, 5 (2009) 7. Times Cited: 43 [Correlational analysis, a novel approach to genetic analysis that Mogil and I first applied to pain in 1999, is applied here to whole-genome data]
5. Abulafia R., Zalkind V, Devor M. Cerebral activity during the anesthesia-like state induced by mesopontine microinjection of pentobarbital. J. Neuroscience, 29 (2009) 7053-64. Times Cited: 19 [This paper maps changes in brain activity upon MPTA microinjection using c-Fos]
6. Devor, M. Ectopic discharge in A? afferents as a source of neuropathic pain. Experimental brain research 196 (2009)115-128. Times Cited:196 [The paper opposes the belief that pain is a matter of C-fibers alone]
7. Kovalsky Y, Amir R, Devor M. Subthreshold oscillations facilitate neuropathic spike discharge by overcoming membrane accommodation. Experimental Neurology 210 (2008) 194-206.. Times Cited: 18 [Subthreshold oscillations in DRGs, that we discovered in 2002, are fundamental to ectopic discharge. This paper shows why]
8. Fried K, Sessle BJ, Devor M. The paradox of pain from tooth pulp: low-threshold "algoneurons"? Pain. 2011 Dec;152:2685-9.
9. Devor, M., Neuropathic pain: pathophysiological response of nerves to injury. Chapter 61. In: S.L. McMahon, M. Koltzenburg, I. Tracey and D.C. Turk (Eds.), Wall and Melzack's Textbook of Pain, 6th edition, Churchill Livingstone, London, 2013, pp 861-888. [Leading textbook in the pain field to which I have contributed since the 1st edition, published 1984]
10. Vaso A, Adahan HM, Gjika A, Zahaj S, Zhurda T, Vyshka G, Devor M. Peripheral nervous system origin of phantom limb pain. Pain 155 (2014) 1384-91. Times Cited: 36 [Data show that phantom limb pain (in humans) is not due to dysfunctional cortical plasticity, but ectopic discharge originating in DRGs.]
11. Sukhotinsky I, Minert A, Soja P, Devor M. Mesopontine switch for the induction of general anesthesia by dedicated neural pathways. Anesth Analg. (2016) [Reviews research on the MPTA since my group discovered it in 2001]
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