Linked Life Data

12764087

Source:http://linkedlifedata.com/resource/pubmed/id/12764087

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2003-5-23
pubmed:abstractText
The possible involvement of p38 mitogen-activated protein kinase activation in spinal cord and dorsal root ganglion (DRG) cells in the development of peripheral neuropathic pain has been explored. Ligation of the L5 spinal nerve (SNL) on one side in adult rats produces an early onset and long-lasting mechanical allodynia. This lesion results in activation of p38 in the L5 segment of the spinal cord, most prominently in the ipsilateral dorsal horn, starting soon after the lesion (<1 d) and persisting for >3 weeks. The activated p38 in the spinal cord is restricted entirely to microglia; phospho-p38 colocalizes only with the microglial marker OX-42 and not with either the neuronal marker neuronal-specific nuclear protein or the astrocyte marker GFAP. In contrast, SNL induces a delayed (>3 d) activation of p38 in the L5 DRG that occurs predominantly in neurons. Continuous injection of the p38 inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580) via the intrathecal route, starting before the SNL surgery, reduces SNL-induced mechanical allodynia from day 1 to day 10, with maximal effects at early time points. Post-treatment with SB203580 starting on day 1 or on day 10 after surgery also reduces established mechanical allodynia. Because the reduction in neuropathic pain by p38 inhibition occurs before the appearance of p38 activation in DRG neurons, p38 activation in spinal cord microglia is likely to have a substantial role in the earliest phase of neuropathic pain. Coactivation of p38 in DRG neurons and spinal microglia may contribute to later phases of neuropathic pain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4017-22
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12764087-Animals, pubmed-meshheading:12764087-Behavior, Animal, pubmed-meshheading:12764087-Enzyme Activation, pubmed-meshheading:12764087-Enzyme Inhibitors, pubmed-meshheading:12764087-Ganglia, Spinal, pubmed-meshheading:12764087-Hyperalgesia, pubmed-meshheading:12764087-Imidazoles, pubmed-meshheading:12764087-Injections, Spinal, pubmed-meshheading:12764087-Ligation, pubmed-meshheading:12764087-Male, pubmed-meshheading:12764087-Microglia, pubmed-meshheading:12764087-Mitogen-Activated Protein Kinases, pubmed-meshheading:12764087-Pain, pubmed-meshheading:12764087-Pain Measurement, pubmed-meshheading:12764087-Pyridines, pubmed-meshheading:12764087-Rats, pubmed-meshheading:12764087-Rats, Sprague-Dawley, pubmed-meshheading:12764087-Spinal Cord, pubmed-meshheading:12764087-Spinal Nerves, pubmed-meshheading:12764087-p38 Mitogen-Activated Protein Kinases
pubmed:year
2003
pubmed:articleTitle
p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain.
pubmed:affiliation
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.