ArticleMolecular pain2007
Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice.
Article in Molecular pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
The trial behind it
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Who cites it
49 citing papers in PubMed, 105 citations in OpenAlex.
- Trial
- Agmatine inhibits NMDA receptor-mediated calcium transients in mouse spinal cord dorsal horn via intact PSD95-nNOS signaling.The Journal of pharmacology and experimental therapeutics · 2024Article
- Brain nuclei and neural circuits in neuropathic pain and brain modulation mechanisms of acupuncture: a review on animal-based experimental research.Frontiers in neuroscience · 2023Review
- Pharmacogenetic inhibition of lumbosacral sensory neurons alleviates visceral hypersensitivity in a mouse model of chronic pelvic pain.PloS one · 2022Article
- Neuropathic Pain: Biomolecular Intervention and Imaging via Targeting Microglia Activation.Biomolecules · 2021Review
- Prospects for the Personalized Multimodal Therapy Approach to Pain Management via Action on NO and NOS.Molecules (Basel, Switzerland) · 2021Review
- Leptin Contributes to Neuropathic Pain via Extrasynaptic NMDAR-nNOS Activation.Molecular neurobiology · 2021Article
- Nitric oxide and sickle cell disease-Is there a painful connection?Experimental biology and medicine (Maywood, N.J.) · 2021Review
- In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain.Molecules (Basel, Switzerland) · 2020Review
- Sleep deficiency and chronic pain: potential underlying mechanisms and clinical implications.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Review
- Targeting nNOS ameliorates the severe neuropathic pain due to chronic pancreatitis.EBioMedicine · 2019Article
- Chronic Pain: Structural and Functional Changes in Brain Structures and Associated Negative Affective States.International journal of molecular sciences · 2019Review
- Effects of Repetitive Transcranial Magnetic Stimulation on Astrocytes Proliferation and nNOS Expression in Neuropathic Pain Rats.Current medical science · 2018Article
- Spinal Circuits for Touch, Pain, and Itch.Annual review of physiology · 2018Review
- Endogenous nitric oxide inhibits spinal NMDA receptor activity and pain hypersensitivity induced by nerve injury.Neuropharmacology · 2017Article
- Indoleamine 2,3-dioxygenase and inducible nitric oxide synthase mediate immune tolerance induced by CTLA4Ig and anti-CD154 hematopoietic stem cell transplantation in a sensitized mouse model.Experimental and therapeutic medicine · 2017Article
- Zerumbone Alleviates Neuropathic Pain through the Involvement of l-Arginine-Nitric Oxide-cGMP-K⁺ ATP Channel Pathways in Chronic Constriction Injury in Mice Model.Molecules (Basel, Switzerland) · 2017Article
- Neuronal plasticity of trigeminal ganglia in mice following nerve injury.Journal of pain research · 2017Article
- Roles of nitric oxide and ethyl pyruvate after peripheral nerve injury.Inflammation and regeneration · 2017Review
- How Nitric Oxide Increases in Diabetic Morphine Tolerated Male Rats.Iranian journal of pharmaceutical research : IJPR · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal nitric oxide synthase (nNOS) is a key enzyme for nitric oxide production in neuronal tissues and contributes to the spinal central sensitization in inflammatory pain. However, the role of nNOS in neuropathic pain remains unclear. The present study combined a genetic strategy with a pharmacologic approach to examine the effects of genetic knockout and pharmacologic inhibition of nNOS on neuropathic pain induced by unilateral fifth lumbar spinal nerve injury in mice. In contrast to wildtype mice, nNOS knockout mice failed to display nerve injury-induced mechanical hypersensitivity. Furthermore, either intraperitoneal (100 mg/kg) or intrathecal (30 microg/5 microl) administration of L-NG-nitro-arginine methyl ester, a nonspecific NOS inhibitor, significantly reversed nerve injury-induced mechanical hypersensitivity on day 7 post-nerve injury in wildtype mice. Intrathecal injection of 7-nitroindazole (8.15 microg/5 microl), a selective nNOS inhibitor, also dramatically attenuated nerve injury-induced mechanical hypersensitivity. Western blot analysis showed that the expression of nNOS protein was significantly increased in ipsilateral L5 dorsal root ganglion but not in ipsilateral L5 lumbar spinal cord on day 7 post-nerve injury. The expression of inducible NOS and endothelial NOS proteins was not markedly altered after nerve injury in either the dorsal root ganglion or spinal cord. Our findings suggest that nNOS, especially in the dorsal root ganglion, may participate in the development and/or maintenance of mechanical hypersensitivity after nerve injury.
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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.