J.D. Levine
National Institutes of Health
16 Papers
332 Citations
J.D. Levine is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Extravasation & Nicotine. The author has an hindex of 12, co-authored 16 publications.
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Papers
Sensory neuropeptide interactions in the production of plasma extravasation in the rat.
TL;DR: It is suggested that galanin and somatostatin inhibit, presynaptically, the release of substance P and calcitonin gene-related peptide from primary afferent terminals to provide a novel mechanism for the regulation ofPrimary afferent neurogenic inflammation.
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Further substantiation of a significant role for the sympathetic nervous system in inflammation
TL;DR: It is shown that bradykinin is able to release norepinephrine in the knee-joint, indicating action on the sympathetic postganglionic neuron, and substantial additional evidence supporting a significant contribution of the sympatheticPostganglionics neuron terminal to inflammatory plasma extravasation is provided.
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Modulation of bradykinin-induced plasma extravasation in the rat knee joint by sympathetic co-transmitters
TL;DR: The data show that sympathetic post-ganglionic neuron-derived mediators may either inhibit or enhance plasma extravasation induced by bradykinin, and it is hypothesize that differential release of mediators from the sympatheticPost-gangLionic neuron terminal, in response to varying stimuli, regulates local plasmaExtravasation during inflammation.
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Central terminals of nociceptors are targets for nicotine suppression of inflammation.
TL;DR: The hypothesis that the central terminal of the primary afferent nociceptor is a CNS target at which nicotine acts to inhibit inflammation is supported.
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•Journal Article
Differential contribution of descending controls to the antinociceptive actions of kappa and mu opioids: an analysis of formalin-evoked C-fos expression.
TL;DR: Results provide the first evidence that supraspinal kappa receptor-mediated antinociception is not dependent on the integrity of the dorsolateral funiculus and may be mediated exclusively at the suPRaspinal level, suggesting that there are multiple mechanisms through which opioids can evoke antinOCiceptive effects.
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