ArticleInflammation2012
Nitric oxide modulated the expression of DREAM/calsenilin/KChIP3 in inflammatory pain of rats.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Neuromeric Distribution of Nicotinamide Adenine Dinucleotide Phosphate-Diaphorase Activity in the Adult Lamprey Brain.Frontiers in neuroanatomy · 2022Article
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- Downstream Regulatory Element Antagonist Modulator (DREAM), a target for anti-thrombotic agents.Pharmacological research · 2017Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Downstream regulatory element antagonistic modulator (DREAM) is a critical transcriptional repressor for pain modulation. The role of nitric oxide (NO) plays in modulating DREAM pain pathway in the periphery is unclear. Therefore, we investigated the role of the NO in modulation of the expression of DREAM in formalin-induced rat inflammatory pain models. Male Sprague-Dawley rats were randomly distributed into four groups: the normal group, formalin test group, Nω-nitro-L-arginine (l-NNA) group, and morphine group. One hundred microliters of 2.5 % formalin was injected into the plantar surface of the right hindpaw of rats. l-NNA (40 nmol/L) and morphine (40 nmol/L) were injected intrathecally in the hindpaw before formalin injection. The nociceptive behavioral reaction was recorded. After the formalin test, the expression of DREAM mRNA and protein in the spinal cord of the four groups were measured. The nociceptive reaction induced by injection of formalin exhibited two phases. Morphine and l-NNA significantly decreased pain scores of the second phase. The expression of DREAM was significantly increased in the rat spinal cord after formalin-induced pain. Morphine significantly upregulated the expression of DREAM, and the formalin-induced upregulation was significantly attenuated by l-NNA. NO may play an important role in the DREAM pathway modulation of inflammatory pain.
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