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Deletion of the neu...
Deletion of the neuropeptide Y Y1 receptor affects pain sensitivity, neuropeptide transport and expression, and dorsal root ganglion neuron numbers.
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- Shi, T-J S (författare)
- Karolinska Institutet
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- Li, J (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
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- Dahlström, Annica, 1941 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
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- Theodorsson, Elvar, 1953- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Avdelningen för klinisk kemi,Klinisk kemi
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- Ceccatelli, S (författare)
- Karolinska Institutet
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Decosterd, I (författare)
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Pedrazzini, T (författare)
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- Hökfelt, Tomas (författare)
- Karolinska Institutet
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(creator_code:org_t)
- Elsevier BV, 2006
- 2006
- Engelska.
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Ingår i: Neuroscience. - : Elsevier BV. - 0306-4522 .- 1873-7544. ; 140:1, s. 293-304
- Relaterad länk:
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https://gup.ub.gu.se...
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https://doi.org/10.1...
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http://kipublication...
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https://urn.kb.se/re...
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Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- 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
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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