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Mohab M. Ibrahim

Researcher at University of Arizona

Publications -  54
Citations -  4086

Mohab M. Ibrahim is an academic researcher from University of Arizona. The author has contributed to research in topics: Chronic pain & Neuropathic pain. The author has an hindex of 23, co-authored 42 publications receiving 3692 citations.

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CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids.

TL;DR: Test the hypothesis that CB(2) receptor activation stimulates release from keratinocytes of the endogenous opioid beta-endorphin, which then acts at local neuronal mu-opioid receptors to inhibit nociception and indicates anatomical specificity of opioid effects.
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Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: Pain inhibition by receptors not present in the CNS

TL;DR: AM1241 dose-dependently reversed tactile and thermal hypersensitivity produced by ligation of the L5 and L6 spinal nerves in rats, demonstrating a mechanism leading to the inhibition of pain, one that targets receptors localized exclusively outside the CNS.
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CB2 cannabinoid receptor-mediated peripheral antinociception.

TL;DR: Using AM1241, a CB2 receptor‐selective agonist, it is demonstrated that CB2 receptors produce antinociception to thermal stimuli and the local, peripheral nature of CB2 cannabinoid antinOCiception is demonstrated.
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Dynorphin Promotes Abnormal Pain and Spinal Opioid Antinociceptive Tolerance

TL;DR: The data suggest that spinal dynorphin promotes abnormal pain and acts to reduce the antinociceptive efficacy of spinal opioids (i.e., tolerance), and identify a possible mechanism for previously unexplained clinical observations and offer a novel approach for the development of strategies that could improve the long-term use of opioids for pain.
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Regular exercise reverses sensory hypersensitivity in a rat neuropathic pain model: role of endogenous opioids.

TL;DR: Regular moderate aerobic exercise reversed signs of neuropathic pain and increased endogenous opioid content in brainstem regions important in pain modulation and suggested that exercise-induced reversal of neuropathy pain results from an up-regulation of endogenous opioids.