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Journal article
Enhanced nociceptive behavior and expansion of associated primary afferents in a rabbit model of cerebral palsy
Journal of neuroscience research, v 100(10), pp 1951-1966
Oct 2022
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Spastic cerebral palsy (CP) is a movement disorder marked by hypertonia and hyperreflexia; the most prevalent comorbidity is pain. Since spinal nociceptive afferents contribute to both the sensation of painful stimuli as well as reflex circuits involved in movement, we investigated the relationship between prenatal hypoxia–ischemia (HI) injury which can cause CP, and possible changes in spinal nociceptive circuitry. To do this, we examined nociceptive afferents and mechanical and thermal sensitivity of New Zealand White rabbit kits after prenatal HI or a sham surgical procedure. As described previously, a range of motor deficits similar to spastic CP was observed in kits born naturally after HI (40 min at ~70%–80% gestation). We found that HI caused an expansion of peptidergic afferents (marked by expression of calcitonin gene‐related peptide) in both the superficial and deep dorsal horn at postnatal day (P)5. Non‐peptidergic nociceptive afferent arborization (labeled by isolectin B4) was unaltered in HI kits, but overlap of the two populations (peptidergic and non‐peptidergic nociceptors) was increased by HI. Density of glial fibrillary acidic protein was unchanged within spinal cord white matter regions important in nociceptive transmission at P5. We found that mechanical and thermal nociception was enhanced in HI kits even in the absence of motor deficits. These findings suggest that prenatal HI injury impacts spinal sensory pathways in addition to the more well‐established disruptions to descending motor circuits. In conclusion, changes to spinal nociceptive circuitry could disrupt spinal reflexes and contribute to pain experienced by individuals with CP.
Most individuals with cerebral palsy (CP) experience pain, yet it is understudied. We demonstrate altered distribution of nociceptive afferents in the dorsal horn of neonatal rabbits that experienced hypoxic–ischemic injury in utero; these anatomical changes were associated with nocifensive behavior indicative of pain. Our findings suggest that CP‐causative injuries alter spinal sensory pathways (not only descending motor circuits), contributing to increased pain in CP.
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Details
- Title
- Enhanced nociceptive behavior and expansion of associated primary afferents in a rabbit model of cerebral palsy
- Creators
- Emily J. Reedich - University of Rhode IslandLandon T. Genry - University of Rhode IslandMeredith A. Singer - Drexel UniversityClarissa Fantin Cavarsan - University of Rhode IslandElvia Mena Avila - University of Rhode IslandDaphne M. Boudreau - University of Rhode IslandMichael C. Brennan - University of Rhode IslandAlyssa M. Garrett - University of Rhode IslandLisa Dowaliby - University of Rhode IslandMegan R. Detloff - Drexel UniversityKatharina A. Quinlan - University of Rhode Island
- Publication Details
- Journal of neuroscience research, v 100(10), pp 1951-1966
- Publisher
- Wiley
- Number of pages
- 16
- Grant note
- NIH NIGMS (P20GM103430) NIH NINDS (NS097880; NS104436) University of Rhode Island
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy
- Web of Science ID
- WOS:000825617800001
- Scopus ID
- 2-s2.0-85134063014
- Other Identifier
- 991019168691404721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Neurosciences