ArticleScientific reports2017
Enhancing excitatory activity of somatosensory cortex alleviates neuropathic pain through regulating homeostatic plasticity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Immediate Consequences of a Spinal Cord Injury During Development: Unique Insights From Ex Vivo Models.Neural plasticity · 2026Review
- Neural signature of chronic migraine mice model and related photophobia in the primary visual cortex.The journal of headache and pain · 2025Article
- Neural mechanisms underlying reduced nocifensive sensitivity in autism-associated Shank3 mutant dogs.Molecular psychiatry · 2025Article
- The dorsal column nuclei scale mechanical sensitivity in naive and neuropathic pain states.Cell reports · 2025Article
- Neuroplasticity in chronic pain: insights into diagnosis and treatment.The Korean journal of pain · 2025Article
- Neuromodulation with transcranial direct current stimulation contributes to motor function recovery via microglia in spinal cord injury.Scientific reports · 2024Article
- Review
- Graph theory analysis reveals an assortative pain network vulnerable to attacks.Scientific reports · 2023Article
- Repetitive and compulsive behavior after Early-Life-Pain associated with reduced long-chain sphingolipid species.Cell & bioscience · 2023Article
- Primary somatosensory cortex bidirectionally modulates sensory gain and nociceptive behavior in a layer-specific manner.Nature communications · 2023Article
- Electroacupuncture Induces Bilateral S1 and ACC Epigenetic Regulation of Genes in a Mouse Model of Neuropathic Pain.Biomedicines · 2023Article
- White matter microstructural alterations in patients with neuropathic pain after spinal cord injury: a diffusion tensor imaging study.Frontiers in neurology · 2023Article
- Homeostatic plasticity and excitation-inhibition balance: The good, the bad, and the ugly.Current opinion in neurobiology · 2022Review
- Novel Therapies for the Treatment of Neuropathic Pain: Potential and Pitfalls.Journal of clinical medicine · 2022Review
- Dissecting the Neural Circuitry for Pain Modulation and Chronic Pain: Insights from Optogenetics.Neuroscience bulletin · 2022Review
- Altered synaptic connections and inhibitory network of the primary somatosensory cortex in chronic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Review
- Optogenetics: Emerging strategies for neuropathic pain treatment.Frontiers in neurology · 2022Review
- Analgesia effect of lentivirus-siSCN9A infected neurons in vincristine induced neuropathic pain rats.Bioengineered · 2021Article
- Rapid volume pulsation of the extracellular space coincides with epileptiform activity in mice and depends on the NBCe1 transporter.The Journal of physiology · 2021Article
- Neural Plasticity in the Brain during Neuropathic Pain.Biomedicines · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
Central sensitization and network hyperexcitability of the nociceptive system is a basic mechanism of neuropathic pain. We hypothesize that development of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in response to lesion-induced somatosensory deprivation and activity loss, and can be controlled by enhancing cortical activity. In a mouse model of neuropathic pain, in vivo two-photon imaging and patch clamp recording showed initial loss and subsequent recovery and enhancement of spontaneous firings of somatosensory cortical pyramidal neurons. Unilateral optogenetic stimulation of cortical pyramidal neurons both prevented and reduced pain-like behavior as detected by bilateral mechanical hypersensitivity of hindlimbs, but corpus callosotomy eliminated the analgesic effect that was ipsilateral, but not contralateral, to optogenetic stimulation, suggesting involvement of inter-hemispheric excitatory drive in this effect. Enhancing activity by focally blocking cortical GABAergic inhibition had a similar relieving effect on the pain-like behavior. Patch clamp recordings from layer V pyramidal neurons showed that optogenetic stimulation normalized cortical hyperexcitability through changing neuronal membrane properties and reducing frequency of excitatory postsynaptic events. We conclude that development of neuropathic pain involves abnormal homeostatic activity regulation of somatosensory cortex, and that enhancing cortical excitatory activity may be a novel strategy for preventing and controlling neuropathic pain.
Indexed as
Identifiers
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.