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. 



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


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

  • Identified a critical period for regeneration of severed axons in the olfactory cortex and patterns of neuroplastic axonal reoganization.

  • Among the first research on collateral sprouting in the skin following nerve injury (rats & humans).

  • 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.

  • Established ectopic discharge in nerve end neuromas as a fundamental factor in neuropathic pain.

  • Demonstrated that corticosteroids and anticonvulsants suppress ectopia and hence neuropathic pain.

  • 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).

  • Establishment of the first animal model of neuropathic pain, the “neuroma model”, still widely used.

  • Discovered the contribution of Na+ channel accumulation in axons to hyperexcitability and neuropathic pain.

  • First demonstration of ephaptic crosstalk at nerve injury sites, previously only a medical speculation.

  • Selection-line strains were used to establish that susceptibility to neuro-pathic pain is heritable; a foundational discovery of "Pain Genetics".

  • First use of correlational analysis for defining fundamental pain “types”.

  • Identification of Cacng2 (stargazin) as a susceptibility gene for neuro-pathic pain (animals and man).

  • Novel mechanism and potential treatment of osteoarthritic pain based intrinsic innervation & dental root canal analogy.

  •  “Ignition Hypothesis” of pain paroxysms in Trigeminal Neuralgia.

  • Discovery of chemically-mediated non-ephaptic/ non-synaptic crosstalk among injured afferent axons and DRG somata.

  • Discovered neuropathic hyperexcitability in DRG neurons and the role of subthreshold oscillations in DRG ectopia.

  • "Algoneurons" defined as neurons whose activity evokes the experience of pain (contrasting with "nociceptors", defined by their receptive field).

  • Discovered the brainstem MPTA, a key node in the network sub-serving brain-state transitions induced by  GABAergic anesthetic agents. 

  • First direct evidence that phantom limb sensation and phantom limb pain in human amputees is driven primarily from the DRG.

  • Novel hypothesis concerning the causes of pain in herpes zoster and postherpetic neuralgia.

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:

The Hebrew University

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