Secondary Pathology of the Thalamus after Focal Cortical Stroke in Rats is not Associated with Thermal or Mechanical Hypersensitivity and is Not Alleviated by Intra-Thalamic Post-Stroke Delivery of Recombinant CDNF or MANF

Autor: Suvi Pöyhönen, Mikko Airavaara, Jenni E. Anttila
Přispěvatelé: Institute of Biotechnology, Neuroscience Center, University Management
Rok vydání: 2019
Předmět:
Male
lcsh:Medicine
NEUROTROPHIC FACTOR MANF
PAIN HYPERSENSITIVITY
law.invention
Rats
Sprague-Dawley
0302 clinical medicine
Thalamus
central post-stroke pain
SYNAPTIC PLASTICITY
law
CDNF/MANF FAMILY
Stroke
0303 health sciences
distal middle cerebral artery occlusion
ISCHEMIC-STROKE
medicine.anatomical_structure
Hyperalgesia
Recombinant DNA
SPINAL-CORD
medicine.symptom
Biomedical Engineering
Inflammation
03 medical and health sciences
ischemic stroke
medicine
Animals
hyperalgesia
030304 developmental biology
Transplantation
DIFFUSION CHANGES
business.industry
lcsh:R
3112 Neurosciences
Original Articles
Cell Biology
MICROGLIAL ACTIVATION
Spinal cord
medicine.disease
CEREBRAL-ARTERY OCCLUSION
Rats
PROGENITOR CELLS
nervous system
inflammation
Synaptic plasticity
Post stroke
business
Neuroscience
030217 neurology & neurosurgery
Zdroj: Cell Transplantation
Cell Transplantation, Vol 28 (2019)
ISSN: 1555-3892
0963-6897
DOI: 10.1177/0963689719837915
Popis: A stroke affecting the somatosensory pathway can trigger central post-stroke pain syndrome (CPSP). The symptoms often include hyperalgesia, which has also been described in rodents after the direct damage of the thalamus. Previous studies have shown that hemorrhagic stroke or ischemia caused by vasoconstriction in the thalamus induces increased pain sensitivity. We investigated whether inducing secondary damage in the thalamus by a cortical stroke causes similar pain hypersensitivity as has previously been reported with direct ischemic injury. We induced a focal cortical ischemia-reperfusion injury in male rats, quantified the amount of secondary neurodegeneration in the thalamus, and measured whether the thalamic neurodegeneration is associated with thermal or mechanical hypersensitivity. After one month, we observed extensive neuronal degeneration and found approximately 40% decrease in the number of NeuN+ cells in the ipsilateral thalamus. At the same time, there was a massive accumulation—a 30-fold increase—of phagocytic cells in the ipsilateral thalamus. However, despite the evident damage in the thalamus, we did not observe thermal or mechanical sensitization. Thus, thalamic neurodegeneration after cortical ischemia-reperfusion does not induce CPSP-like symptoms in rats, and these results suggest that direct ischemic damage is needed for CPSP induction. Despite not observing hyperalgesia, we investigated whether administration of cerebral dopamine neurotrophic factor (CDNF) and mesencephalic astrocyte-derived neurotrophic factor (MANF) into the ipsilateral thalamus would reduce the secondary damage. We gave a single injection (10 µg) of recombinant CDNF or MANF protein into the thalamus at 7 days post-stroke. Both CDNF and MANF treatment promoted the functional recovery but had no effect on the neuronal loss or the amount of phagocytic cells in the thalamus.
Databáze: OpenAIRE
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