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Tetrodotoxin-resistant Na+ Currents and Inflammatory Hyperalgesia
Pages 7645-7649

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From page 7645...
... Hyperalgesia that develops in the Presence of tissue injury or inflammation reflects, at least in part, an increase in the excitability of high-threshold primary afferent neurons inner vating the site of injury. The increase in afferent excitability, or sensitization, develops within minutes of an inflammatory stimulus and involves a leftward shift in neuronal stimulus response function and/or an increase in spontaneous activity.
From page 7646...
... The distribution and biophysical properties of the classically described TTXresistant Na+ currents suggests that these currents are involved in the control of the excitability of primary afferent neurons. Furthermore, several inflammatory mediators released in response to injury are capable of directly sensitizing subpopulations of primary afferent neurons (9, 10, 14, 42, 43~.
From page 7647...
... had previously demonstrated that the intrathecal administration of ODNs could be used to knock down expression of proteins present in the peripheral terminals of primary afferent neurons. Therefore, we generated antisense ODNs to a unique region of the cloned TTX-resistant Na+ channel, PN3/SNS, and assessed the effects of intrathecal ODN administration on PGE2-induced hyperalgesia (66~.
From page 7648...
... In their carefully controlled study, Porreca et al. were able to demonstrate profound effects with antisense ODN treatment on hyperalgesia resulting from the peripheral administration of Freund's adjuvant.
From page 7649...
... (1994) Brain Res.


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