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Deletion of the neu...
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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 ...
Nummerbeteckningar
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LIBRIS-ID:oai:gup.ub.gu.se/61016
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https://gup.ub.gu.se/publication/61016URI
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https://doi.org/10.1016/j.neuroscience.2006.02.009DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:1942441URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-35676URI
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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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
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Animals
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Axotomy
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methods
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Behavior
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Animal
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Biological Transport
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genetics
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Calcitonin Gene-Related Peptide
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genetics
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metabolism
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Cell Count
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methods
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Functional Laterality
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Ganglia
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Spinal
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cytology
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Gene Expression
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genetics
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Immunohistochemistry
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methods
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In Situ Hybridization
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methods
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Male
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Mice
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Mice
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Inbred C57BL
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Mice
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Knockout
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Neurons
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drug effects
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metabolism
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Neuropeptides
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metabolism
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Pain Measurement
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methods
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Pain Threshold
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drug effects
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physiology
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Posterior Horn Cells
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metabolism
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Receptors
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Neuropeptide Y
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deficiency
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Substance P
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genetics
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metabolism
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MEDICINE
Biuppslag (personer, institutioner, konferenser, titlar ...)
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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)
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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)
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Theodorsson, Elvar,1953-Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Avdelningen för klinisk kemi,Klinisk kemi(Swepub:liu)elvth65
(författare)
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Ceccatelli, SKarolinska Institutet
(författare)
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Decosterd, I
(författare)
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Pedrazzini, T
(författare)
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Hökfelt, TomasKarolinska Institutet
(författare)
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Karolinska InstitutetInstitutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Neuroscience: Elsevier BV140:1, s. 293-3040306-45221873-7544
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