| Literature DB >> 26415594 |
Yuxin Ma1, Chang Zhou1, Guoying Li1, Yinghong Tian2, Jing Liu1, Li Yan1, Yuyun Jiang1, Sumin Tian3.
Abstract
Neuropathic pain and cognitive deficit are frequently comorbidity in clinical, but their underlying correlation and mechanisms remain unclear. Here, we utilized a combined rat model including kainic acid (KA) injection into bilateral striatal marginal division and chronic constriction nerve injury (CCI). PET/CT scans revealed that the SUVmax of KA rats was significantly decreased when compared to naive and saline rats. In contrast to the naive and saline rats, KA rats had longer latencies in locating the hidden platform on day 4, 5 in Morris water maze task. Thermal hyperalgesia and mechanical allodynia of KA rats were alleviated following CCI. Immunostaining results showed that substance P was markedly increased within ipsilateral spinal cord dorsal horn of KA rats after CCI, especially on the post-operative day 14. By means of real-time PCR, the up-regulation of GluR within ipsilateral spinal cord dorsal horn was observed in all KA and CCI rats. PKCγ, IL-6 and NF-κB were up-regulated in both CCI rats when compared to naive and their respective sham rats. These results suggest that cognitive impairment of rats altered the pain behaviors, and these intracellular regulators play crucial roles in the process of neuropathic pain.Entities:
Keywords: Cognitive deficit; Kainic acid; Marginal division; Neuropathic pain; Spinal cord
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Year: 2015 PMID: 26415594 DOI: 10.1007/s11064-015-1727-6
Source DB: PubMed Journal: Neurochem Res ISSN: 0364-3190 Impact factor: 3.996