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Neuro? Logical! Forum for all neuro-things => from neuron to brain...

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Old 25-10-2009, 02:10 PM   #1
Mike Hoy
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Default New Sci Am

I just received the November issue of SciAm and there is an article on "New Culprits in Chronic Pain". Looks interesting.
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Old 25-10-2009, 02:41 PM   #2
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I was unable to read the article, but found there has been much recent information in the research on the subject of the contributions of Glial cells to neuropathic pain. Looks like animal models mostly, but treatment from a direct interruption of the glial cells' contributions following a n. injury (MAPK) appears to reduce pain as per one of many articles on the subject:

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Brain Nerve. 2008 May;60(5):483-92 [Contribution of primary sensory neurons and spinal glial cells to pathomechanisms of neuropathic pain]

Injury to the peripheral nerves often induces produces spontaneous pain, hyperalgesia (increased responsiveness to noxious stimuli), and allodynia (painful responses to normally innocuous stimuli). In contrast to inflammatory pain, the currently available therapeutics for neuropathic pain are either relatively ineffective or accompanied by considerable side effects. Numerous animal models of chronic pain following nerve injury have been introduced. All these neuropathic pain models are generated by partial nerve injury, where a few primary afferents are axotomized, while the others are spared. Among these models, the L5 spinal nerve ligation (SNL) model is unique because in this model, the L4 dorsal root ganglion (DRG) neurons are clearly separated from the axotomized L5 DRG neurons. Previous studies have focused considerable attention on the directly damaged primary afferents and their influence on the activity of the dorsal horn neurons. However, increasing evidence suggests that DRG neurons with intact axons also exhibit alterad excitability and gene expression, and these changes might play functional roles in the pathomechanisms of neuropathic pain. For example, L5 SNL increases the expression of substance P, calcitonin gene-related peptide, brain-derived neurotrophic factor, and the transient receptor potential ion channels TRPV1 and TRPA1 in the uninjured L4 DRG neurons. Furthermore, compelling evidence suggests that the glial cells in the spinal cord may also play a role in the pathogenesis of neuropathic pain. Recent studies have shown that peripheral nerve injury results in the activation of mitogen-activated protein kinases (MAPK) in spinal glial cells and that MAPK inhibitors diminish nerve injury-induced pain hypersensitivity. This review mainly focuses on the DRG neurons and spinal glial cells and will review the roles of MAPK in the nociceptive pathways for neuropathic pain.
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Old 25-10-2009, 04:25 PM   #3
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It's good that other researchers are batting this idea around. Linda Watson was the first, I think, to look at microglial contribution to pain states, 2003. If you use the search function here, you'll find a bunch of stuff on glia.
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