Linked Life Data

12114291

Source:http://linkedlifedata.com/resource/pubmed/id/12114291

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-7-12
pubmed:abstractText
Inflammation in the joint causes peripheral sensitization (increase of sensitivity of nociceptive primary afferent neurons) and central sensitization (hyperexcitability of nociceptive neurons in the central nervous system). The processes of sensitization are thought to be the basis of arthritic pain that appears as spontaneous pain (joints at rest) and hyperalgesia (augmented pain response on noxious stimulation and pain on normally nonpainful stimulation). Sensitization also facilitates efferent neuronal processes through which the nervous system influences the inflammatory process. Peripheral sensitization is produced by the action of inflammatory mediators such as bradykinin, prostaglandins, neuropeptides, and cytokines which activate corresponding receptors in proportions of nerve fibers. In addition, the expression of receptors, for example, bradykinin and neurokinin 1 receptors, is upregulated during inflammation. The development of hyperexcitability of spinal cord neurons is produced by various transmitter/receptor systems that constitute and modulate synaptic activation of the neurons. The key transmitter is glutamate that activates N-methyl-d-aspartate (NMDA) and non-NMDA receptors on spinal cord neurons. Blockade of these receptors prevents and reduces central sensitization. Excitatory neuropeptides (substance P and calcitonin gene-related peptide) further central sensitization. Central sensitization also is facilitated by mediators that have complex actions (e.g., prostaglandin E(2)). Spinal PGE(2) binds to receptors at presynaptic endings of primary afferent neurons (thus influencing synaptic release) and to receptors on postsynaptic spinal cord neurons. The administration of PGE(2) to the spinal cord surface produces changes of responsiveness of spinal neurons similar to peripheral inflammation, and spinal indomethacin to the spinal cord attenuates development of hyperexcitability significantly.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
966
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-54
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed-meshheading:12114291-Afferent Pathways, pubmed-meshheading:12114291-Analgesics, Non-Narcotic, pubmed-meshheading:12114291-Animals, pubmed-meshheading:12114291-Arthritis, pubmed-meshheading:12114291-Cyclooxygenase Inhibitors, pubmed-meshheading:12114291-Dinoprostone, pubmed-meshheading:12114291-Efferent Pathways, pubmed-meshheading:12114291-Ganglia, Spinal, pubmed-meshheading:12114291-Glutamic Acid, pubmed-meshheading:12114291-Humans, pubmed-meshheading:12114291-Hyperalgesia, pubmed-meshheading:12114291-Inflammation Mediators, pubmed-meshheading:12114291-Ion Channel Gating, pubmed-meshheading:12114291-Mechanoreceptors, pubmed-meshheading:12114291-Models, Biological, pubmed-meshheading:12114291-Neuropeptides, pubmed-meshheading:12114291-Nociceptors, pubmed-meshheading:12114291-Pain, pubmed-meshheading:12114291-Rats, pubmed-meshheading:12114291-Receptors, Neuropeptide, pubmed-meshheading:12114291-Receptors, Neurotransmitter, pubmed-meshheading:12114291-Receptors, Prostaglandin E, pubmed-meshheading:12114291-Spinal Cord
pubmed:year
2002
pubmed:articleTitle
Mechanisms of pain in arthritis.
pubmed:affiliation
Department of Physiology, Friedrich-Schiller University of Jena, Jena, Germany. schaible@mti-n.uni-jena.de
pubmed:publicationType
Journal Article, Review