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"We also observed the
previously described NGF-induced increase in Nav1.8 amplitudes in small diameter
IB4 /caps neurons, though in our hands, this effect
was not statistically significant, which may be attributed to the rather small
samples size of these cells in our study (Figure 6(e) and (f))."
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"NGF can be released upon tissue inflammation and is implicated in chronic pain.47 NGF sensitizes nociceptors and promotes their excitability by up-regulating TRPV1 and Nav1.8 channel expression and activity via acting on the TrkA receptor.48,49 In a previous study, Cheng et al4 found that TNF-α produced from ipsilateral injured DRG of a rat spinal nerve ligation model can diffuse to the contralateral side via cerebrospinal fluid and activates satellite cells to produce NGF, which promotes nociceptor excitability on the contralateral side and induces MIP."
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"Thus, NGF acts via TrkA and p75 to activate a number of other kinase pathways, for example, that of p38 kinase, leading to altered gene transcription and increased synthesis of sensory neuropeptides (substance P, CGRP), ion channels (TRPV1, NaV1.8, ASIC3) [141-143], membrane receptors such as bradykinin and P2X3 [144,145], and structural molecules, including neurofilament and channel anchoring proteins such as the annexin light chain p11 [121]."