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Sökning: onr:"swepub:oai:gup.ub.gu.se/61016" > Deletion of the neu...

  • Shi, T-J SKarolinska Institutet (författare)

Deletion of the neuropeptide Y Y1 receptor affects pain sensitivity, neuropeptide transport and expression, and dorsal root ganglion neuron numbers.

  • Artikel/kapitelEngelska2006

Förlag, utgivningsår, omfång ...

  • Elsevier BV,2006

Nummerbeteckningar

  • LIBRIS-ID:oai:gup.ub.gu.se/61016
  • https://gup.ub.gu.se/publication/61016URI
  • https://doi.org/10.1016/j.neuroscience.2006.02.009DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:1942441URI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-35676URI

Kompletterande språkuppgifter

  • Språk:engelska

Ingår i deldatabas

Klassifikation

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

Anmärkningar

  • Neuropeptide Y has been implicated in pain modulation and is substantially up-regulated in dorsal root ganglia after peripheral nerve injury. To identify the role of neuropeptide Y after axotomy, we investigated the behavioral and neurochemical phenotype of neuropeptide Y Y1 receptor knockout mice with focus on dorsal root ganglion neurons and spinal cord. Using a specific antibody Y1 receptor immunoreactivity was found in dorsal root ganglia and in dorsal horn neurons of wild-type, but not knockout mice. The Y1 receptor knockout mice exhibited a pronounced mechanical hypersensitivity. After sciatic nerve axotomy, the deletion of Y1 receptor protected knockout mice from the axotomy-induced loss of dorsal root ganglion neurons seen in wild-type mice. Lower levels of calcitonin gene-related peptide and substance P were identified by immunohistochemistry in dorsal root ganglia and dorsal horn of knockout mice, and the axotomy-induced down-regulation of both calcitonin gene-related peptide and substance P was accentuated in Y1 receptor knockout. However, the transcript levels for calcitonin gene-related peptide and substance P were significantly higher in knockout than in wild-type dorsal root ganglia ipsilateral to the axotomy, while more calcitonin gene-related peptide- and substance P-like immunoreactivity accumulated proximal and distal to a crush of the sciatic nerve. These results indicate that the deletion of the Y1 receptor causes increased release and compensatory increased synthesis of calcitonin gene-related peptide and substance P in dorsal root ganglion neurons. Together, these findings suggest that, after peripheral nerve injury, neuropeptide Y, via its Y1 receptor receptor, plays a key role in cell survival as well as in transport and synthesis of the excitatory dorsal horn messengers calcitonin gene-related peptide and substance P and thus may contribute to pain hypersensitivity.

Ämnesord och genrebeteckningar

  • Animals
  • Axotomy
  • methods
  • Behavior
  • Animal
  • Biological Transport
  • genetics
  • Calcitonin Gene-Related Peptide
  • genetics
  • metabolism
  • Cell Count
  • methods
  • Functional Laterality
  • Ganglia
  • Spinal
  • cytology
  • Gene Expression
  • genetics
  • Immunohistochemistry
  • methods
  • In Situ Hybridization
  • methods
  • Male
  • Mice
  • Mice
  • Inbred C57BL
  • Mice
  • Knockout
  • Neurons
  • drug effects
  • metabolism
  • Neuropeptides
  • metabolism
  • Pain Measurement
  • methods
  • Pain Threshold
  • drug effects
  • physiology
  • Posterior Horn Cells
  • metabolism
  • Receptors
  • Neuropeptide Y
  • deficiency
  • Substance P
  • genetics
  • metabolism
  • MEDICINE

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

  • Li, JGothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology (författare)
  • Dahlström, Annica,1941Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology(Swepub:gu)xdahla (författare)
  • Theodorsson, Elvar,1953-Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Avdelningen för klinisk kemi,Klinisk kemi(Swepub:liu)elvth65 (författare)
  • Ceccatelli, SKarolinska Institutet (författare)
  • Decosterd, I (författare)
  • Pedrazzini, T (författare)
  • Hökfelt, TomasKarolinska Institutet (författare)
  • Karolinska InstitutetInstitutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Neuroscience: Elsevier BV140:1, s. 293-3040306-45221873-7544

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