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  • Holm, LovisaLinköpings universitet,Klinisk kemi,Hälsouniversitetet (författare)

Effects of intracerebroventricular galanin or a galanin receptor 2/3 agonist on the lesion induced by transient occlusion of the middle cerebral artery in female rats

  • Artikel/kapitelEngelska2011

Förlag, utgivningsår, omfång ...

  • Elsevier Science B.V., Amsterdam,2011
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:liu-66126
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-66126URI
  • https://doi.org/10.1016/j.npep.2010.09.002DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:121953758URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Several studies have shown that injury to the central and peripheral nervous system can increase expression of galanin, a 29 amino acid neuropeptide. Moreover, there is evidence that galanin, especially through its galanin receptor 2 (GalR2) receptor, plays a neuroprotective role in different injury models. However, direct studies of a possible neuroprotective effect of galanin in experimental stroke models are lacking. Galanin, a GalR2/3 agonist or artificial CSF was continuously infused intracerebroventricularly (i.c.v.) in naive female rats after a 60 min transient and focal occlusion of the middle cerebral artery. The animals were sacrificed, and the ischemic lesion was visualized using 2,3,5-triphenyltetrazolium hydrochloride (TTC) staining. The lesion was 98% larger after i.c.v, administration of the GalR2/3 agonist (2.4 nmol/day) seven days after occlusion compared to artificial CSF (p = 0.023). No statistically significant differences were found after seven days in the groups treated with galanin in three different concentrations (0.24, 2.4 and 24 nmol/day; p = 0.939, 0.715 and 0.977, respectively). There was no difference in the size of the ischemic lesions measured after three days in the galanin-treated group (2.4 nmol/d) compared to artificial CSF (p = 0.925). The present results show, surprisingly, that a GalR2/3 agonist doubled the size of the ischemic lesion. Whether this effect primarily reflects the properties of the current model, species, gender and/or the mode of galanin administration, e.g. causing desensitization, or whether galanin indeed lacks neuroprotective effect of its own, remains to be corroborated.

Ämnesord och genrebeteckningar

  • Cerebral ischemia
  • Neuropeptide
  • Neuroprotection
  • Stroke
  • MEDICINE
  • MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Theodorsson, ElvarÖstergötlands Läns Landsting,Linköpings universitet,Klinisk kemi,Hälsouniversitetet(Swepub:liu)elvth65 (författare)
  • Hokfelt, TomasKarolinska Institutet (författare)
  • Theodorsson, AnnetteÖstergötlands Läns Landsting,Linköpings universitet,Klinisk kemi,Hälsouniversitetet,Neurokirurgiska kliniken US(Swepub:liu)annth93 (författare)
  • Linköpings universitetKlinisk kemi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Neuropeptides: Elsevier Science B.V., Amsterdam45:1, s. 17-230143-41791532-2785

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