Professor Michael Tal
born: 1947 (Jerusalem, Israel)
Department of Medical Neurobiology
Faculty of Medicine, Hebrew University of Jerusalem
Ein Kerem, Jerusalem 91010
Web page and http://www.ipa.org.il
Tal is a laboratory head and the president of The Israel Pain
Association. His higher education was at Hebrew University (DMD) and
UCLA (MS). He had worked for 2 years with Gary Bennett at NIH and recently
withRon Dubner and Ken Ren In Baltimore Maryland. His laboratory has
published in the pain field, with work of a notably integrative nature
involving neurophysiology, psychophysiology and animal behavior.
1. Mechanisms of neuropathic pain after nerve injury. Mechanisms whereby injury
evokes sensory dysfunction and chronic pain. Pathophysiology of injured nerve,
particularly, abnormal discharge originates at the site of nerve injury or
in the DRG in experimental animal models for neuropathy in
2. Relationship between sensory and motor modalities in the oro-facial area.
Effects and mechanisms of different drugs and hypnosis on pain and reflexes
in the oro-facial area.
Sample of recent research publications:
- The transition from naive to primed nociceptive state: A novel wind-up protocol in mice.
Ziv NY, Tal M, Shavit Y. Exp Neurol. 2015 Oct 9;275P3:133-142.
- Adi Nitzan-Luques, Marshall Devor and Michael Tal. (2013) Dynamic genotype-selective "phenotypic switching" of CGRP expression contributes to differential neuropathic pain phenotype. Exp. Neurol. 25;250C:194-204.
- Matthias Ringkamp, Michael Tal, Timothy V. Hartke, Matthew Wooten, Alvin McKelvy, Brian P Turnquist, Yun Guan, Richard A. Meyer, Srinivasa N. Raja. (2012) Local loperamide injection reduces mechanosensitivity of rat cutaneous, nociceptive C- fibers. PLoS ONE, 7(7):e42105.
- Chronic blockade of interleukin-1 (IL-1) prevents and attenuates neuropathic pain behavior and spontaneous ectopic neuronal activity following nerve injury.
Gabay E, Wolf G, Shavit Y, Yirmiya R, Tal M.
Eur J Pain. 2011 Mar;15(3):242-8.
- Genotype-selective phenotypic switch in primary afferent neurons contributes to neuropathic pain.
Nitzan-Luques A, Devor M, Tal M.
Pain. 2011 Oct;152(10):2413-26.
- Eran Gabay, Gilly Wolf, Yehuda Shavit, Raz Yirmiya, Michael Tal. (2010) Chronic Blockade of Interleukin-1 (IL-1) Prevents and Attenuates Neuropathic Pain Behavior and Spontaneous Ectopic Neuronal Activity Following Nerve Injury. European J of Pain, August 26.
- Jonathan Nissenbaum, Marshall Devor, Ze'ev Seltzer, Mathias Gebauer, Martin Michaelis, Michael Tal, Ruslan Dorfman, Merav Abitbul-Yarkoni, Yan Lu, Sonia delCanho, Anne Minert, Kaj Fried, Anna-Karin Persson, Hagai Shpigler1, Benjamin Yakir, Anne Pisante, Ariel Darvasi (2010). Susceptibility to chronic pain following nerve injury is genetically controlled by CACNG2. Genome Research. Sep;20(9):1180-90.
- What causes low back pain ? Marshall Devor and Michael Tal Editorial. (2009) Pain 142,(1),11-12.
- Eli Eliav, Rafael Benoliel, Uri Herzberg, Mythili Kalladka and Michael Tal (2009) The Role of IL-6 and
IL-1beta in Painful Perineural Inflammatory Neuritis. Brain, Behavior, and Immunity. 23 (2009) 474-484.
- Dan Kaufmann, Boris Yagen, Anne Minert, Michael Tal, Marshall Devor and Meir Bialer (2008). Evaluation of the Enantioselective Antiallodynic and Pharmacokinetic Profile of Propylisopropylacetamide, a Chiral Isomer of Valproic Acid Amide. Neuropharmacology, Mar;54(4):699-707.
- Kleibeuker, W, Gabay, E., Kavelaars, A., Zijlstra, J., Wolf, G., Ziv, N., Yirmiya, R.,Shavit, Y.,
Tal, M., and Heijnen, C. J.: (2007). IL-1? signaling is required for mechanical allodynia induced by nerve injury and for the ensuing reduction in spinal cord neuronal GRK2. Brain Behav. Immun. 22(2):200-8.
- Tal M, Kim J, Back SK, Na HS, Devor M (2006) Onset of ectopic fring in the Chung model of neuropathic pain coincides with the onset of tactile allodynia. In: Flor H, Kalso E, Dostrovsky JO
(eds), Proceedings of the 11th world congress on pain, IASP Press, Seattle, pp 119-130
- Wolf, G., Gabay, E., Tal, M., Yirmiya, R., Shavit, Y. (2006) Impairment of Interleukin-1 (IL-1) Signaling Attenuates Neuropathic Pain and Spontaneous Ectopic Neuronal Activity Following Nerve Injury. Pain 120:315-324
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