uu.seUppsala universitets publikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Spinal nerve lesion alters blood-spinal cord barrier function and activates astrocytes in the rat
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
2006 (engelsk)Inngår i: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 124, nr 1-2, s. 211-221Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Alterations in the spinal cord microenvironment in a neuropathic pain model in rats comprising right L-4 spinal nerve lesion were examined following 1, 2, 4 and 10 weeks using albumin and glial fibrillary acidic protein (GFAP) immunoreactivity. Rats subjected to nerve lesion showed pronounced activation of GFAP indicating astrocyte activation, and exhibited marked leakage of albumin, suggesting defects of the blood-spinal cord barrier (BSCB) function in the corresponding spinal cord segment. The intensities of these changes were most prominent in the gray matter of the lesioned side compared to them contralateral cord in both the dorsal and ventral horns. The most marked changes in albumin and GFAP inummoreaction were seen after 2 weeks and persisted with mild intensities even after 10 weeks. Distortion of nerve cells, loss of neurons and general sponginess were evident in the gray matter of the spinal cord corresponding to the lesion side. These nerve cell and glial cell changes are mainly evident in the areas showing leakage of endogenous albumin in the spinal cord. These novel observations indicate that chronic nerve lesion has the capacity to induce a selective increase in local BSCB permeability that could be instrumental in nerve cell and glial cell activation. These findings may be relevant to our current understanding on the pathophysiology of neuropathic pain.

sted, utgiver, år, opplag, sider
2006. Vol. 124, nr 1-2, s. 211-221
Emneord [en]
nerve lesion, neuropathic pain, blood-spinal cord barrier permeability, astrocytes, glial fibrillary acidic protein immunoreactivity, albumin extravasation, spinal cord microenvironment, neuronal damage
HSV kategori
Identifikatorer
URN: urn:nbn:se:uu:diva-82044DOI: 10.1016/j.pain.2006.05.020ISI: 000240581700030PubMedID: 16806707OAI: oai:DiVA.org:uu-82044DiVA, id: diva2:109959
Tilgjengelig fra: 2006-09-12 Laget: 2006-09-12 Sist oppdatert: 2017-12-14bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

Andre lenker

Forlagets fulltekstPubMed

Personposter BETA

Gordh, TorstenSharma, Hari Shanker

Søk i DiVA

Av forfatter/redaktør
Gordh, TorstenSharma, Hari Shanker
Av organisasjonen
I samme tidsskrift
Pain

Søk utenfor DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric

doi
pubmed
urn-nbn
Totalt: 577 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf