Brain research
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Nerve growth factor (NGF) reverses some effects of axotomy and prevents toxic neuropathy in adult rodents. We tested the effect of NGF on behavioral hyperalgesia resulting from a chronic constriction injury (CCI) of the sciatic nerve in the rat [5]. CCI rats exhibit thermal hyperalgesia as demonstrated by a reduction of paw withdrawal latency to a noxious thermal stimulus applied to the paw on the side of injury. ⋯ Infusion of NGF on the sciatic nerve of rats that had no CCI had no significant effect on paw withdrawal latency. Infusion of anti-NGF antiserum did not enhance hyperalgesia in CCI rats. These results suggest that alterations in neurotrophic factor(s) contribute to the development of behavioral hyperalgesia in an animal model of neuropathy and that NGF may have therapeutic value in the treatment of neuropathic pain in humans.
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Regional levels of phosphatidylinositol 4,5-bisphosphate (PIP2), diacylglycerol (DG) and free fatty acids (FFA), involved in the signal transduction pathway of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue PIP2 concentrations were significantly reduced in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Only levels of stearic and arachidonic acids were substantially decreased in PIP2 in these regions of the brain. ⋯ At 20 min postinjury, a significant decrease in PIP2 concentration and significant increases in levels of DG and FFA were observed only in the injured left cortex. In addition to the increases in stearic and arachidonic acids in FFA, increased amounts of palmitic and oleic acids were also found in the injured left cortex at 20 min after injury. These results suggest that the PIP2 signal transduction pathway is activated in the cortex and hippocampus at the onset of lateral FP brain injury and that the enhanced phospholipase C-catalyzed phosphodiestric breakdown of PIP2 is a major mechanism of liberation of FFA in these sites immediately after such injury.