ArticleJournal of neuroinflammation2022
Coexistence of chronic hyperalgesia and multilevel neuroinflammatory responses after experimental SCI: a systematic approach to profiling neuropathic pain.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- Role of Supraspinal Neuroinflammation in Chronic Pain After Experimental Spinal Cord Injury-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Impact of vitamin D on the prognosis after spinal cord injury: A systematic review.Frontiers in nutrition · 2023Pooled it
- Spinal cord stimulation: An emerging strategy for chronic pain relief after spinal cord injury.Neural regeneration research · 2026Article
- The basolateral amygdala decodes visceral pain and itch via distinct circuits and molecules.Nature communications · 2026Article
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- Thermodynamic Biomarkers of Neuroinflammation: Nanothermometry, Energy-Stress Dynamics, and Predictive Entropy in Glial-Vascular Networks.International journal of molecular sciences · 2025Review
- The dorsal column nuclei encode and transmit the network signatures of mechanical allodynia.Cell reports · 2025Article
- Astrocytic Inducible Nitric Oxide Synthase Upregulation Contributes to Chronic Below-Level Neuropathic Pain Following Spinal Cord Injury in Male Rats.European journal of pain (London, England) · 2025Article
- An engineering-reinforced extracellular vesicle-integrated hydrogel with an ROS-responsive release pattern mitigates spinal cord injury.Science advances · 2025Article
- Repeated Administrations of Polyphenolic Extracts Prevent Chronic Reflexive and Non-Reflexive Neuropathic Pain Responses by Modulating Gliosis and CCL2-CCR2/CX3CL1-CX3CR1 Signaling in Spinal Cord-Injured Female Mice.International journal of molecular sciences · 2025Article
- SGK1 upregulation in GFAPCell death & disease · 2025Article
- Neuropathic Pain Induced by Spinal Cord Injury from the Glia Perspective and Its Treatment.Cellular and molecular neurobiology · 2024Review
- Article
- Combined transplantation of hiPSC-NSC and hMSC ameliorated neuroinflammation and promoted neuroregeneration in acute spinal cord injury.Stem cell research & therapy · 2024Article
- Article
- Review
- Transient Reflexive Pain Responses and Chronic Affective Nonreflexive Pain Responses Associated with Neuroinflammation Processes in Both Spinal and Supraspinal Structures in Spinal Cord-Injured Female Mice.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPeople with spinal cord injury (SCI) frequently develop neuropathic pain (NP) that worsens disability and diminishes rehabilitation efficacy. Chronic NP is presently incurable due to poor understanding of underlying mechanisms. We hypothesized that multilocus neuroinflammation (NIF) might be a driver of SCI NP, and tested it by investigating whether NP coexisted with central NIF, neurotransmission (NTM), neuromodulation (NML) and neuroplasticity (NPL) changes post-SCI.
methodsFemale Sprague-Dawley rats (230-250 g) with T10 compression or laminectomy were evaluated for physical conditions, coordinated hindlimb functions, neurological reflexes, and mechanical/thermal sensitivity thresholds at 1 day post-injury (p.i.) and weekly thereafter. Eight weeks p.i., central nervous system tissues were histochemically and immunohistochemically characterized for parameters/markers of histopathology and NIF/NTM/NML/NPL. Also analyzed was the correlative relationship between levels of selected biomarkers and thermosensitivity thresholds via statistical linear regression.
resultsSCI impaired sensorimotor functions, altered reflexes, and produced spontaneous pain signs and hypersensitivity to evoked nociceptive, mechanical, and thermal inputs. Only injured spinal cords exhibited neural lesion, microglia/astrocyte activation, and abnormal expression of proinflammatory cytokines, as well as NIF/NTM/NML/NPL markers. Brains of SCI animals displayed similar pathophysiological signs in the gracile and parabrachial nuclei (GrN and PBN: sensory relay), raphe magnus nucleus and periaqueduct gray (RMN and PAG: pain modulation), basolateral amygdala (BLA: emotional-affective dimension of pain), and hippocampus (HPC: memory/mood/neurogenesis). SCI augmented sensory NTM/NPL (GrN and PBN); increased GAD67 (PAG) level; reduced serotonin (RMN) and fear-off neuronal NTR2 (BLA) expressions; and perturbed neurogenesis (HPC).
conclusionT10 compression caused chronic hyperalgesia that coexisted with NIF/NTM/NML/NPL responses at multilevel neuroaxis centers. The data have provided multidimensional biomarkers as new mechanistic leads to profile SCI NP for therapeutic/therapy development.
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