Bone cancer induces a unique central sensitization through synaptic changes in a wide area of the spinal cord - Wikidata - wikimedia - TriplyDB

Bone cancer induces a unique central sensitization through synaptic changes in a wide area of the spinal cord

Bone cancer induces a unique central sensitization through synaptic changes in a wide area of the spinal cord

http://www.wikidata.org/entity/Q34489274

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The Physiology of Bone Pain. How Much Do We Really Know?Bone cancer pain: from mechanism to therapy Palliation of bone cancer pain by antagonists of platelet-activating factor receptors Dissociation between the relief of skeletal pain behaviors and skin hypersensitivity in a model of bone cancer pain.Alleviation of behavioral hypersensitivity in mouse models of inflammatory pain with two structurally different casein kinase 1 (CK1) inhibitors.PAR2-mediated upregulation of BDNF contributes to central sensitization in bone cancer pain.The neurobiology of cancer pain.Enhanced GABAergic synaptic transmission at VLPAG neurons and potent modulation by oxycodone in a bone cancer pain model.Preventive or late administration of anti-NGF therapy attenuates tumor-induced nerve sprouting, neuroma formation, and cancer pain.Activation of c-jun N-terminal kinase in spinal cord contributes to breast cancer induced bone pain in rats.Activation of spinal MrgC-Gi-NR2B-nNOS signaling pathway by Mas oncogene-related gene C receptor agonist bovine adrenal medulla 8-22 attenuates bone cancer pain in mice.Minocycline attenuates bone cancer pain in rats by inhibiting NF-κB in spinal astrocytes.Pathobiology and management of prostate cancer-induced bone pain: recent insights and future treatments.Dorsal horn interneuron-derived Netrin-4 contributes to spinal sensitization in chronic pain via Unc5B.Differences in electrophysiological properties of functionally identified nociceptive sensory neurons in an animal model of cancer-induced bone pain Mediation of Movement-Induced Breakthrough Cancer Pain by IB4-Binding Nociceptors in Rats.Metastatic human breast cancer to the spine produces mechanical hyperalgesia and gait deficits in rodents.Brain-derived neurotrophic factor modulates N-methyl-D-aspartate receptor activation in a rat model of cancer-induced bone pain.Rat model of cancer-induced bone pain: changes in nonnociceptive sensory neurons in vivo.Mice with cancer-induced bone pain show a marked decline in day/night activity.Activation of PI3Kγ/Akt pathway mediates bone cancer pain in rats.Analgesic Effect of Intrathecal Administration of Chemokine Receptor CCR2 Antagonist is Related to Change in Spinal NR2B, nNOS, and SIGIRR Expression in Rat with Bone Cancer Pain.

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Bone cancer induces a unique central sensitization through synaptic changes in a wide area of the spinal cord

http://www.wikidata.org/entity/Q34489274

description

2010 nî lūn-bûn

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Bone cancer induces a unique c ...... a wide area of the spinal cord

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Bone cancer induces a unique c ...... a wide area of the spinal cord

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Daisuke Uta

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Hidemasa Furue

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Jun Yamamoto

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Keiji Imoto

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Megumu Yoshimura

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Shingo Furuse

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Tomoyuki Kawamata

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Toshihiko Katafuchi

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Yoshikazu Yanagisawa

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Yukihide Iwamoto

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P2860

Long-term potentiation depends on release of D-serine from astrocytes.

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

Origins of skeletal pain: sensory and sympathetic innervation of the mouse femur.

Malignant bone pain: pathophysiology and treatment.

Ca2+-permeable AMPA receptors in synaptic plasticity and neuronal death.

Tumor-evoked hyperalgesia and sensitization of nociceptive dorsal horn neurons in a murine model of cancer pain.

The role of N-methyl-D-aspartate receptor subunit NR2B in spinal cord in cancer pain.

A rat model of bone cancer pain.

Differential activation of spinal cord glial cells in murine models of neuropathic and cancer pain.

Bone cancer increases transient receptor potential vanilloid subfamily 1 expression within distinct subpopulations of dorsal root ganglion neurons.

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