ArticleNeuroscience2016
Post-translational modification of cortical GluA receptors in rodents following spinal cord lesion.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- AMPA receptors play an important role in the biological consequences of spinal cord injury: Implications for AMPA receptor modulators for therapeutic benefit.Biochemical pharmacology · 2024Review
- Rehabilitation Training after Spinal Cord Injury Affects Brain Structure and Function: From Mechanisms to Methods.Biomedicines · 2023Review
- Central neuropathic pain.Nature reviews. Disease primers · 2023Review
- Central Neuropathic Pain Syndromes: Current and Emerging Pharmacological Strategies.CNS drugs · 2022Review
- Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- Botulinum Toxin for Central Neuropathic Pain.Toxins · 2018Review
- Loss of dopamine D1 receptors and diminished D1/5 receptor-mediated ERK phosphorylation in the periaqueductal gray after spinal cord lesion.Neuroscience · 2017Article
- Plasticity in respiratory motor neurons in response to reduced synaptic inputs: A form of homeostatic plasticity in respiratory control?Experimental neurology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies investigating the pathophysiology of neuropathic pain caused by injury to the spinal cord suggest that pain may result, at least in part, from maladaptive plasticity in the somatosensory cortex and associated pain networks. However, little is known about the molecular and cellular mechanisms leading to maladaptive plasticity in the cortex and how they contribute to the development of neuropathic pain. AMPA-type glutamate receptors (GluARs) mediate fast excitatory synaptic transmission in the mammalian brain and play an important role in pain processing. Here we used an electrolytic lesion model of spinal cord injury in animals to study the expression and phosphorylation of GluA1 and 2 in the primary somatosensory cortex (S1). Experiments in rats and mice revealed that maladaptive plasticity and hypersensitivity after spinal cord lesion (SCL) are associated with a reduction in the fraction of GluA1 subunits that are phosphorylated at serine 831 (S831) in the hindlimb representation of S1 (S1HL). Manipulations that reduce the fraction of phosphorylated S831 in S1HL of non-lesioned animals, including low-frequency electrical stimulation and viral-mediated gene transfer of mutant S831, were associated with the development of hypersensitivity. Taken together, these findings suggest that phosphorylation of GluA1 at S831 plays an important role in the development of hypersensitivity after SCL.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.