Caspase-3 activity is reduced after spinal cord injury in mice lacking dynorphin: differential effects on glia and neurons

↓ Direkt till sidans innehåll
↓ Direkt till sidans sekundära innehåll (sidomenyn)

Search: onr:"swepub:oai:DiVA.org:uu-120092" > Caspase-3 activity ...

1 of 1
Previous record
Next record
To hitlist

Details
MARC

Adjan, V. V.Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA (author)

Caspase-3 activity is reduced after spinal cord injury in mice lacking dynorphin : differential effects on glia and neurons

Article/chapterEnglish2007

Publisher, publication year, extent ...

Elsevier BV,2007
printrdacarrier

Numbers

LIBRIS-ID:oai:DiVA.org:uu-120092
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120092URI
https://doi.org/10.1016/j.neuroscience.2007.05.053DOI
http://kipublications.ki.se/Default.aspx?queryparsed=id:115973801URI

Supplementary language notes

Language:English
Summary in:English

Part of subdatabase

SwePubSwePub

Classification

Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

Notes

Dynorphins are endogenous opioid peptide products of the prodynorphin gene. An extensive literature suggests that dynorphins have deleterious effects on CNS injury outcome. We thus examined whether a deficiency of dynorphin would protect against tissue damage after spinal cord injury (SCI), and if individual cell types would be specifically affected. Wild-type and prodynorphin(-/-) mice received a moderate contusion injury at 10th thoracic vertebrae (T10). Caspase-3 activity at the injury site was significantly decreased in tissue homogenates from prodynorphin(-/-) mice after 4 h. We examined frozen sections at 4 h post-injury by immunostaining for active caspase-3. At 3-4 mm rostral or caudal to the injury, >90% of all neurons, astrocytes and oligodendrocytes expressed active caspase-3 in both wild-type and knockout mice. At 6-7 mm, there were fewer caspase-3(+) oligodendrocytes and astrocytes than at 3-4 mm. Importantly, caspase-3 activation was significantly lower in prodynorphin(-/-) oligodendrocytes and astrocytes, as compared with wild-type mice. In contrast, while caspase-3 expression in neurons also declined with further distance from the injury, there was no effect of genotype. Radioimmunoassay showed that dynorphin A(1-17) was regionally increased in wild-type injured versus sham-injured tissues, although levels of the prodynorphin processing product Arg(6)-Leu-enkephalin were unchanged. Our results indicate that dynorphin peptides affect the extent of post-injury caspase-3 activation, and that glia are especially sensitive to these effects. By promoting caspase-3 activation, dynorphin peptides likely increase the probability of glial apoptosis after SCI. While normally beneficial, our findings suggest that prodynorphin or its peptide products become maladaptive following SCI and contribute to secondary injury.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Farmakologi och toxikologi hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Pharmacology and Toxicology hsv//eng
apoptosis
astrocyte
excitotoxic cell death
oligodendrocyte
glutamate
traumatic injury
Biological research on drug dependence
Biologisk beroendeforskning
MEDICINE
MEDICIN

Added entries (persons, corporate bodies, meetings, titles ...)

Hauser, K. F.Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA and Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, USA (author)
Bakalkin, GeorgyExperimental Alcohol and Drug Addiction Research Section, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden,Molecular neuropsychopharmacology(Swepub:uu)gueba200 (author)
Yakovleva, T.Experimental Alcohol and Drug Addiction Research Section, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden,Molecular neuropsychopharmacology(Swepub:uu)tatia678 (author)
Gharibyan, A.Experimental Alcohol and Drug Addiction Research Section, Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden (author)
Scheff, S. W.Department of Anatomy and Neurobiology, 800 Rose Street, MS209, University of Kentucky, Lexington, KY 40536-0298, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536-0298, USA and Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536-0298, USA (author)
Knapp, P. E.Department of Anatomy and Neurobiology, 800 Rose Street, MS209, University of Kentucky, Lexington, KY 40536-0298, USA and Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536-0298, USA (author)
Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USADepartment of Anatomy and Neurobiology, University of Kentucky, Lexington, USA and Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, USA (creator_code:org_t)

Related titles

In:Neuroscience: Elsevier BV148:3, s. 724-360306-45221873-7544

Internet link

Find in a library

Neuroscience (Search for host publication in LIBRIS)

To the university's database

1 of 1
Previous record
Next record
To hitlist

Find more in SwePub

By the author/editor: Adjan, V. V.; Hauser, K. F.; Bakalkin, Georgy; Yakovleva, T.; Gharibyan, A.; Scheff, S. W.; show more...; Knapp, P. E.; show less...

About the subject

MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Basic Medicine; and Pharmacology and ...

Articles in the publication: Neuroscience

By the university: Uppsala University; Karolinska Institutet

Search outside SwePub

Extend your search to:: Google; Google Book Search; Google Scholar

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

LIBRIS.kb.se