J. Levine

Publications
Influence

The capsaicin receptor: a heat-activated ion channel in the pain pathway

M. Caterina, M. Schumacher, M. Tominaga, Tobias A. Rosen, J. Levine, D. Julius
Biology
Nature
22 October 1997

The cloned capsaicin receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo.

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Hyperalgesic agents increase a tetrodotoxin-resistant Na+ current in nociceptors.

M. Gold, D. Reichling, M. Shuster, J. Levine
Biology
Proceedings of the National Academy of Sciences…
6 February 1996

Modulation of TTX-R INa is a mechanism for sensitization of mammalian nociceptors, as indicated by results indicating that three agents that produce tenderness or hyperalgesia in vivo, prostaglandin E2, adenosine, and serotonin, modulate TTx-R Ina.

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Modulation of TTX-R INa by PKC and PKA and Their Role in PGE2-Induced Sensitization of Rat Sensory Neurons In Vitro

M. Gold, J. Levine, A. M. Correa
Biology
The Journal of Neuroscience
15 December 1998

Investigating the interaction between PKC and PKA revealed that although inhibitors of PKA had little effect on PKC-induced modulation of TTX-R INa, inhibitors of PKC significantly attenuated PKA- induced modulation of the current.

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Characterization of six voltage-gated K+ currents in adult rat sensory neurons.

M. Gold, M. Shuster, J. Levine
Biology
Journal of neurophysiology
1 June 1996

Using whole cell patch-clamp techniques, evidence is provided for the existence of six voltage-gated K+ currents in cultured dorsal root ganglion (DRG) neurons from the adult rat, and four of the six currents are differentially expressed among subpopulations of DRG neurons.

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Bradykinin-12-lipoxygenase-VR1 signaling pathway for inflammatory hyperalgesia

Jieun Shin, Hawon Cho, U. Oh
Biology
Proceedings of the National Academy of Sciences…
3 July 2002

Bristolkinin, acting at B2 bradykinin receptors, excites sensory nerve endings by activating capsaicin receptors via production of 12-lipoxygenase metabolites of arachidonic acid, identifying a mechanism that might be targeted in the development of new therapeutic strategies for the treatment of inflammatory pain.

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TRP channels: targets for the relief of pain.