Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice. - Wikidata - awgldk - TriplyDB

Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice.

Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice.

http://www.wikidata.org/entity/Q36162388

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The spinal cord expression of neuronal and inducible nitric oxide synthases and their contribution in the maintenance of neuropathic pain in mice.Development of nitric oxide synthase inhibitors for neurodegeneration and neuropathic pain.Mas-related G-protein-coupled receptors inhibit pathological pain in mice.Involvement of spinal NR2B-containing NMDA receptors in oxaliplatin-induced mechanical allodynia in rats.Preserved acute pain and impaired neuropathic pain in mice lacking protein interacting with C Kinase 1 Hospitalization for pain in patients with sickle cell disease treated with sildenafil for elevated TRV and low exercise capacity.A quantitative study of neuronal nitric oxide synthase expression in laminae I-III of the rat spinal dorsal horn.Nitric oxide inhibits nociceptive transmission by differentially regulating glutamate and glycine release to spinal dorsal horn neurons.Reduction of blood nitric oxide levels is associated with clinical improvement of the chronic pelvic pain related to endometriosis.Induction of spinal long-term synaptic potentiation is sensitive to inhibition of neuronal NOS in L5 spinal nerve-transected rats Reduction of Neuropathic and Inflammatory Pain through Inhibition of the Tetrahydrobiopterin Pathway.The three isoforms of nitric oxide synthase distinctively affect mouse nocifensive behavior Phosphorylated neuronal nitric oxide synthase in neuropathic pain in rats.Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.Role of nitric oxide synthase in the development of bone cancer pain and effect of L-NMMA Dimethylarginine dimethylaminohydrolase 1 is involved in spinal nociceptive plasticity.Proteome of synaptosome-associated proteins in spinal cord dorsal horn after peripheral nerve injury.Peripheral nerve injury up-regulates expression of interactor protein for cytohesin exchange factor 1 (IPCEF1) mRNA in rat dorsal root ganglion.Updated role of nitric oxide in disorders of erythrocyte function.Reduced spinal microglial activation and neuropathic pain after nerve injury in mice lacking all three nitric oxide synthases.PKC-Dependent Signaling Pathways within PAG and Thalamus Contribute to the Nitric Oxide-Induced Nociceptive Behavior.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 Nitric oxide activates ATP-sensitive potassium channels in mammalian sensory neurons: action by direct S-nitrosylation.Dual effect of exogenous nitric oxide on neuronal excitability in rat substantia gelatinosa neurons.Neuronal nitric oxide signaling regulates erection recovery after cavernous nerve injury.Disruption of nNOS-PSD95 protein-protein interaction inhibits acute thermal hyperalgesia and chronic mechanical allodynia in rodents.Complex regulation of the regulator of synaptic plasticity histone deacetylase 2 in the rodent dorsal horn after peripheral injury.How Nitric Oxide Increases in Diabetic Morphine Tolerated Male Rats.Peripheral effects of morphine and expression of μ-opioid receptors in the dorsal root ganglia during neuropathic pain: nitric oxide signaling.Neuronal plasticity of trigeminal ganglia in mice following nerve injury.Participation of neuronal nitric oxide synthase in experimental neuropathic pain induced by sciatic nerve transection.Reversal of NO-induced nociceptive hypersensitivity by St. John's wort and hypericin: NF-κB, CREB and STAT1 as molecular targets.Spinal Circuits for Touch, Pain, and Itch.Endothelial nitric oxide synthase in dorsal root ganglia during chronic inflammatory nociception.Nitric oxide signaling contributes to ectopic orofacial neuropathic pain.Roles of nitric oxide and ethyl pyruvate after peripheral nerve injury.Zerumbone Alleviates Neuropathic Pain through the Involvement of l-Arginine-Nitric Oxide-cGMP-K⁺ ATP Channel Pathways in Chronic Constriction Injury in Mice Model.The furoxan nitric oxide donor, PRG150, evokes dose-dependent analgesia in a rat model of painful diabetic neuropathy

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P2860

Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice.

http://www.wikidata.org/entity/Q36162388

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Genetic knockout and pharmacol ...... ical hypersensitivity in mice.

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Genetic knockout and pharmacol ...... ical hypersensitivity in mice.

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Genetic knockout and pharmacol ...... ical hypersensitivity in mice.

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Myron Yaster

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Srinivasa N Raja

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Yuan-Xiang Tao

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Yun Guan

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P2860

Expression and action of cyclic GMP-dependent protein kinase Ialpha in inflammatory hyperalgesia in rat spinal cord

Impaired NMDA receptor-mediated postsynaptic function and blunted NMDA receptor-dependent persistent pain in mice lacking postsynaptic density-93 protein

Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons.

Nitric oxide as modulator of neuronal function.

Formation of nitric oxide from L-arginine in the central nervous system: a transduction mechanism for stimulation of the soluble guanylate cyclase.

Nitric oxide: first in a new class of neurotransmitters.

Neuronal nitric oxide synthase is upregulated in a subset of primary sensory afferents after nerve injury which are necessary for analgesia from alpha2-adrenoceptor stimulation.

Nitric oxide (NO) and nociceptive processing in the spinal cord.

Neuronal nitric oxide synthase mRNA upregulation in rat sensory neurons after spinal nerve ligation: lack of a role in allodynia development.

Inhibition of spinal protein kinase C reduces nerve injury-induced tactile allodynia in neuropathic rats.

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