ArticleThe Journal of physiology2011
Acute inhibition of signalling phenotype of spinal GABAergic neurons by tumour necrosis factor-alpha.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- TNF-α acutely enhances acid-sensing ion channel currents in rat dorsal root ganglion neurons via a p38 MAPK pathway.Journal of neuroinflammation · 2021Article
- Acute P38-Mediated Enhancement of P2X3 Receptor Currents by TNF-α in Rat Dorsal Root Ganglion Neurons.Journal of inflammation research · 2021Article
- Cytokine inflammatory threat, but not LPS one, shortens GABAergic synaptic currents in the mouse spinal cord organotypic cultures.Journal of neuroinflammation · 2019Article
- Sustained stimulation of βBrain, behavior, and immunity · 2018Article
- Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro.Molecular brain · 2018Article
- Interleukin-1 receptor type 1 is overexpressed in neurons but not in glial cells within the rat superficial spinal dorsal horn in complete Freund adjuvant-induced inflammatory pain.Journal of neuroinflammation · 2017Article
- Involvement of Spinal IL-6 Trans-Signaling in the Induction of Hyperexcitability of Deep Dorsal Horn Neurons by Spinal Tumor Necrosis Factor-Alpha.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Spinal release of tumour necrosis factor activates c-Jun N-terminal kinase and mediates inflammation-induced hypersensitivity.European journal of pain (London, England) · 2015Article
- Ang II-salt hypertension depends on neuronal activity in the hypothalamic paraventricular nucleus but not on local actions of tumor necrosis factor-α.Hypertension (Dallas, Tex. : 1979) · 2014Article
- Immune dysregulation in autism spectrum disorder.European journal of pediatrics · 2014Review
- Dynamic effects of TNF-α on synaptic transmission in mice over time following sciatic nerve chronic constriction injury.Journal of neurophysiology · 2013Article
- Decreased expression and role of GRK6 in spinal cord of rats after chronic constriction injury.Neurochemical research · 2013Article
- Growth factors in synaptic function.Frontiers in synaptic neuroscience · 2013Review
- Induction of thermal hyperalgesia and synaptic long-term potentiation in the spinal cord lamina I by TNF-α and IL-1β is mediated by glial cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Therapeutic role of hematopoietic stem cells in autism spectrum disorder-related inflammation.Frontiers in immunology · 2013Article
- Minocycline blocks lipopolysaccharide induced hyperalgesia by suppression of microglia but not astrocytes.Neuroscience · 2012Article
- Evidence that spinal astrocytes but not microglia contribute to the pathogenesis of Paclitaxel-induced painful neuropathy.The journal of pain · 2012Article
- Modulation of spinal cord synaptic activity by tumor necrosis factor α in a model of peripheral neuropathy.Journal of neuroinflammation · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Spinal application of TNFα induces both allodynia and hyperalgesia, and at least part of the pronociceptive effects of TNFα have been suggested as due to the impaired function of spinal inhibitory neurons (disinhibition). The present study explores the effects of TNFα on the signalling phenotype of spinal GABAergic neurons identified in transgenic mice expressing green fluorescent protein at the glutamic acid decarboxylase 67 (GAD67) promoter. Acute application of TNFα directly inhibits the excitability of a subset of GAD67(+) spinal neurons. TNFα-induced inhibition was dependent on the activation of p38 mitogen-activated protein kinase (MAPK) within these GAD67(+) neurons. TNFα receptor 1 (TNFR1) but not receptor 2 (TNFR2) was identified on spinal GAD67(+) neurons, suggesting that TNFα signals through TNFR1. Voltage-clamp recordings of GAD67(+) neurons indicated that the inhibitory effect of TNFα was through suppression of the hyperpolarization-activated cation current (I(h)). This study defines a novel mechanism of spinal disinhibition mediated by a TNFα-TNFR1-p38 pathway within GABAergic inhibitory interneurons.
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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.