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Suhayl J. Jabbur

Researcher at American University of Beirut

Publications -  97
Citations -  2772

Suhayl J. Jabbur is an academic researcher from American University of Beirut. The author has contributed to research in topics: Hyperalgesia & Nociception. The author has an hindex of 29, co-authored 97 publications receiving 2674 citations. Previous affiliations of Suhayl J. Jabbur include Lebanese University.

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Endotoxin-induced local inflammation and hyperalgesia in rats and mice: a new model for inflammatory pain.

TL;DR: The results indicate that the use of ET‐produced hyperalgesia is a valid model for local and reversible inflammatory pain, with minimal distress to the animal, and can also be used to study the efficacy of various anti‐inflammatory and analgesic drugs and the molecular mechanisms of inflammation induced by bacterial invasion.
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Augmentation of nociceptive reflexes and chronic deafferentation pain by chemical lesions of either dopaminergic terminals or midbrain dopaminergic neurons.

TL;DR: The results suggest that the dopaminergic system plays a major role in the processing of nociceptive information in the striatum and the limbic areas.
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Nociceptive behavior in animal models for peripheral neuropathy: spinal and supraspinal mechanisms.

TL;DR: It is speculated that neuropathic pain, like extrapyramidal motor syndromes, reflects a disorder in the processing of somatosensory information.
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Attenuation of neuropathic pain by segmental and supraspinal activation of the dorsal column system in awake rats

TL;DR: Dorsal column nuclear stimulation, rostral to selective dorsal spinal lesions, produced strong inhibitory effects on the allodynia and hyperalgesia observed in both models of mononeuropathy, comparable to those observed following similar stimulations in rats with an intact spinal cord.
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Spinal segmental and supraspinal mechanisms underlying the pain-relieving effects of spinal cord stimulation: an experimental study in a rat model of neuropathy.

TL;DR: It is suggested that both supraspinal and segmental mechanisms are activated by SCS, and that in this model with DC lesions, rostral and caudal stimulations may activate different synaptic circuitries and transmitter systems.