ArticleBMC neuroscience2014
Differential neuropathic pain sensitivity and expression of spinal mediators in Lewis and Fischer 344 rats.
Article in BMC neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Glutamatergic systems in neuropathic pain and emerging non-opioid therapies.Pharmacological research · 2022Review
- Sciatic nerve injury rebalances the hypothalamic-pituitary-adrenal axis in rats with persistent changes to their social behaviours.Journal of neuroendocrinology · 2022Article
- Chronic Orofacial Pain: Models, Mechanisms, and Genetic and Related Environmental Influences.International journal of molecular sciences · 2021Review
- The influence of rat strain on the development of neuropathic pain and comorbid anxio-depressive behaviour after nerve injury.Scientific reports · 2020Article
- Hypothalamic-pituitary-adrenal axis function in traumatic spinal cord injury-related neuropathic pain: a case-control study.Journal of endocrinological investigation · 2019Article
- The analgesic efficacy of morphine varies with rat strain and experimental pain model: implications for target validation efforts in pain drug discovery.European journal of pain (London, England) · 2019Article
- Review
- The Effect of Ethanolic Extract of Lippia Citriodora on Rats with Chronic Constriction Injury of Neuropathic pain.Cell journal · 2018Article
- Chronic Social Stress Time-Dependently Affects Neuropathic Pain-Related Cold Allodynia and Leads to Altered Expression of Spinal Biochemical Mediators.Frontiers in behavioral neuroscience · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAltered hypothalamo-pituitary-adrenal (HPA) axis activity may be accompanied by a modulation of pain sensitivity. In a model of neuropathic pain (chronic constriction injury, CCI) we investigated the onset and maintenance of mechanical allodynia/hyperalgesia and the expression of biochemical mediators potentially involved in spinal cell modulation in two rat strains displaying either hypo- (Lewis-LEW) or hyper- (Fischer 344-FIS) reactivity of the HPA axis.
resultsMechanical pain thresholds and plasmatic corticosterone levels were assessed before and during periods of 4 or 21 days following CCI surgery. At the end of the respective protocols, the mRNA expression of glial cell markers (GFAP and Iba1) and glutamate transporters (EAAT3 and EAAT2) were examined. We observed a correlation between the HPA axis reactivity and the pain behavior but not as commonly described in the literature; LEW rats seemed to be less sensitive than FIS from 4 to 14 days after the CCI surgery when looking at the mechanical allodynia/hyperalgesia. However, the biochemical spinal markers expression we observed is conflicting.
conclusionWe did not find a specific causal relation between the pain behavior and the glial cell activation or the expression of the glutamate transporters, suggesting that the interaction between the HPA axis and the spinal activation pattern is more complex in a context of neuropathic pain.
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