ArticleBMC neuroscience2008
Persistent changes in spinal cord gene expression after recovery from inflammatory hyperalgesia: a preliminary study on pain memory.
Article in BMC neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Differential Gene Expression in Pain-Related Genes are not Affected by the Presence of Dementia.Pain management nursing : official journal of the American Society of Pain Management Nurses · 2024Article
- Sex Differences in Nociceptor Translatomes Contribute to Divergent Prostaglandin Signaling in Male and Female Mice.Biological psychiatry · 2022Article
- Contribution of COMT and BDNF Genotype and Expression to the Risk of Transition From Acute to Chronic Low Back Pain.The Clinical journal of pain · 2020Article
- Chronic postsurgical pain: is there a possible genetic link?British journal of pain · 2017Article
- Acute Low Back Pain: Differential Somatosensory Function and Gene Expression Compared With Healthy No-Pain Controls.The Clinical journal of pain · 2016Article
- Striatal Plasticity in L-DOPA- and Graft-Induced Dyskinesia; The Common Link?Frontiers in cellular neuroscience · 2016Review
- Epigenetic regulation of persistent pain.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Article
- Descending controls modulate inflammatory joint pain and regulate CXC chemokine and iNOS expression in the dorsal horn.Molecular pain · 2014Article
- Anatomy of Graft-induced Dyskinesias: Circuit Remodeling in the Parkinsonian Striatum.Basal ganglia · 2012Article
- Article
- The synaptic impact of the host immune response in a parkinsonian allograft rat model: Influence on graft-derived aberrant behaviors.Neurobiology of disease · 2008Article
- Article
- Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies found that rats subjected to carrageenan injection develop hyperalgesia, and despite complete recovery in several days, they continue to have an enhanced hyperalgesic response to a new noxious challenge for more than 28d. The study's aim was to identify candidate genes that have a role in the formation of the long-term hyperalgesia-related imprint in the spinal cord. This objective was undertaken with the understanding that the long-lasting imprint of acute pain in the central nervous system may contribute to the transition of acute pain to chronicity.
resultsTo analyze changes in gene expression when carrageenan-induced hyperalgesia has disappeared but propensity for the enhanced hyperalgesic response is still present, we determined the gene expression profile using oligo microarray in the lumbar part of the spinal cord in three groups of rats: 28d after carrageenan injection, 24h after injection (the peak of inflammation), and with no injection (control group). Out of 17,000 annotated genes, 356 were found to be differentially expressed compared with the control group at 28d, and 329 at 24h after carrageenan injection (both groups at p < 0.01). Among differentially expressed genes, 67 (39 in 28d group) were identified as being part of pain-related pathways, altered in different models of pain, or interacting with proteins involved in pain-related pathways. Using gene ontology (GO) classification, we have identified 3 functional classes deserving attention for possible association with pain memory: They are related to cell-to-cell interaction, synaptogenesis, and neurogenesis.
conclusionDespite recovery from inflammatory hyperalgesia, persistent changes in spinal cord gene expression may underlie the propensity for the enhanced hyperalgesic response. We suggest that lasting changes in expression of genes involved in the formation of new synapses and neurogenesis may contribute to the transition of acute pain to chronicity.
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