
The Devor lab
research on chronic pain and pain-free surgery
ABOUT ME
I am most proud of a series of innovative contributions that opened new research avenues and in which my research was the first, or among the first, in the literature. These include:
Prof. Devor has contributed considerably to the understanding of the neurobiological basis of neuropathic pain. More recently he has also investigated mechanisms involved loss of consciousness and pain-free surgery. His laboratory has published extensively in the pain field, with work of a notably integrative nature involving neurophysiology, computer simulations, neuroanatomy (light and electron microscopy), genetics, and behavioral models. He is author of over 300 publications in the field of pain science. >20,000 career citations, h-index 73, i10 index 193.
EDUCATION
RESEARCH INTERESTS
Pain mechansisms, particularly neuropathic pain.
Heritability of pain and pain genetics.
1966 - 1970
Princeton University
A.B., Department of Psychology (minor biology)
Mechanisms of general anaesthesia and the transition from wakefulness to unconsciousness.
Basis of pain-free surgery under general anesthesia.
Development and plasticity in the olfactory cortex.
Nerve growth and regeneration.
Synaptic plasticity and map reorganization in the spinal cord after nerve injury.
1970 - 1975
M.I.T. , Cambridge Mass
Ph.D., Department of Brain & Cognitive Sciences
1975
University College London
Postdoctoral Fellow under Prof. P.D Wall
Motivation: hypothalamic control of hunger and thirst. Self-stimulation reward. Pheromones
1975 -1977
The Hebrew University of Jerusalem
Postdoctoral Fellow under Prof. P.D Wall
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Identified a critical period for regeneration of severed axons in the olfactory cortex and patterns of neuroplastic axonal reoganization.
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Among the first research on collateral sprouting in the skin following nerve injury (rats & humans).
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Discovery of neuroplastic reorganization of somatosensory maps in the spinal dorsal horn and cortex following peripheral nerve injury. This work was subsequently extended by others to primates and humans.
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Established ectopic discharge in nerve end neuromas as a fundamental factor in neuropathic pain.
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Demonstrated that corticosteroids and anticonvulsants suppress ectopia and hence neuropathic pain.
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Discovery of “sympathetic-sensory coupling" as a factor in neuropathic pain, and its association with sympathetic sprouting in the cut nerve end and the dorsal root ganglion (DRG).
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Establishment of the first animal model of neuropathic pain, the “neuroma model”, still widely used.
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Discovered the contribution of Na+ channel accumulation in axons to hyperexcitability and neuropathic pain.
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First demonstration of ephaptic crosstalk at nerve injury sites, previously only a medical speculation.
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Selection-line strains were used to establish that susceptibility to neuro-pathic pain is heritable; a foundational discovery of "Pain Genetics".
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First use of correlational analysis for defining fundamental pain “types”.
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Identification of Cacng2 (stargazin) as a susceptibility gene for neuro-pathic pain (animals and man).
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Novel mechanism and potential treatment of osteoarthritic pain based intrinsic innervation & dental root canal analogy.
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“Ignition Hypothesis” of pain paroxysms in Trigeminal Neuralgia.
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Discovery of chemically-mediated non-ephaptic/ non-synaptic crosstalk among injured afferent axons and DRG somata.
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Discovered neuropathic hyperexcitability in DRG neurons and the role of subthreshold oscillations in DRG ectopia.
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"Algoneurons" defined as neurons whose activity evokes the experience of pain (contrasting with "nociceptors", defined by their receptive field).
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Discovered the brainstem MPTA, a key node in the network sub-serving brain-state transitions induced by GABAergic anesthetic agents.
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First direct evidence that phantom limb sensation and phantom limb pain in human amputees is driven primarily from the DRG.
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Novel hypothesis concerning the causes of pain in herpes zoster and postherpetic neuralgia.
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