ArticleBiomolecules2016
Glutaminase Increases in Rat Dorsal Root Ganglion Neurons after Unilateral Adjuvant-Induced Hind Paw Inflammation.
Article in Biomolecules, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Loss of Glutaminase 1 in Small Sensory Neurons Prevents Nerve Injury Induced Mechanical Allodynia: Insights From Conditional Knockout Mice.European journal of pain (London, England) · 2025Article
- Exploring the Role of RhoA/ROCK Signaling in Pain: A Narrative Review.Aging and disease · 2025Review
- Tubulin Polyglutamylation by TTLL1 and TTLL7 Regulate Glutamate Concentration in the Mice Brain.Biomolecules · 2023Article
- Increase of glutamate in satellite glial cells of the trigeminal ganglion in a rat model of craniofacial neuropathic pain.Frontiers in neuroanatomy · 2023Article
- Peripheral role of glutamate in orofacial pain.Frontiers in neuroscience · 2022Review
- Subcellular localization of neuronal nuclei (NeuN) antigen in size and calcitonin gene-related peptide (CGRP) populations of dorsal root ganglion (DRG) neurons during acute peripheral inflammation.Neuroscience letters · 2021Article
- Open-source method of image cytometry in dorsal root ganglia tissue with immunofluorescence.Analytical biochemistry · 2021Article
- VGLUT2/Cdk5/p25 Signaling Pathway Contributed to Inflammatory Pain by Complete Freund's Adjuvant.Pain research & management · 2020Article
- Glutaminase C Regulates Microglial Activation and Pro-inflammatory Exosome Release: Relevance to the Pathogenesis of Alzheimer's Disease.Frontiers in cellular neuroscience · 2019Article
- Hydroxylated Fullerene: A Stellar Nanomedicine to Treat Lumbar Radiculopathy via Antagonizing TNF-ACS biomaterials science & engineering · 2018Article
- Article
- Glutaminase C overexpression in the brain induces learning deficits, synaptic dysfunctions, and neuroinflammation in mice.Brain, behavior, and immunity · 2017Article
- [RhoA/Rho-kinase contributes to chronic pain following thoracotomy by up-regulating glutaminase 1 expression in rat spinal dorsal cord].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Parkinson's disease: Microglial/macrophage-induced immunoexcitotoxicity as a central mechanism of neurodegeneration.Surgical neurology international · 2017Review
- Characterization of glutamatergic neurons in the rat atrial intrinsic cardiac ganglia that project to the cardiac ventricular wall.Neuroscience · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Glutamate is a neurotransmitter used at both the peripheral and central terminals of nociceptive primary sensory neurons, yet little is known concerning regulation of glutamate metabolism during peripheral inflammation. Glutaminase (GLS) is an enzyme of the glutamate-glutamine cycle that converts glutamine into glutamate for neurotransmission and is implicated in producing elevated levels of glutamate in central and peripheral terminals. A potential mechanism for increased levels of glutamate is an elevation in GLS expression. We assessed GLS expression after unilateral hind paw inflammation by measuring GLS immunoreactivity (ir) with quantitative image analysis of L4 dorsal root ganglion (DRG) neurons after one, two, four, and eight days of adjuvant-induced arthritis (AIA) compared to saline injected controls. No significant elevation in GLS-ir occurred in the DRG ipsilateral to the inflamed hind paw after one or two days of AIA. After four days AIA, GLS-ir was elevated significantly in all sizes of DRG neurons. After eight days AIA, GLS-ir remained elevated in small (<400 µm²), presumably nociceptive neurons. Western blot analysis of the L4 DRG at day four AIA confirmed the elevated GLS-ir. The present study indicates that GLS expression is increased in the chronic stage of inflammation and may be a target for chronic pain therapy.
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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.