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Tumor necrosis factor potentiates central vagal afferent signaling by modulating ryanodine channels.

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Disease processes such as infection, leukemia, and autoimmune disorders are often associated with nausea, emesis, and anorexia. A common denominator of these rather disparate states is the production of the early, proinflammatory cytokine tumor necrosis factor-alpha (TNF) in significant quantities.

The effects of ryanodine receptor (RYR1) mutation on natural killer cell cytotoxicity, plasma cytokines and stress hormones during acute intermittent exercise in pigs.

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Stress susceptibility has been mapped to a single recessive gene, the ryanodine receptor 1 (RYR1) gene or halothane (Hal) gene. Homozygous (Hal(nn)), mutated pigs are sensitive to halothane and susceptible to Porcine Stress Syndrome (PSS). Previous studies have shown that stress-susceptible RYR1

Ryanodine receptor antagonism protects the ischemic liver and modulates TNF-alpha and IL-10.

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BACKGROUND Dantrolene is a ryanodine receptor and intracellular calcium antagonist. The ryanodine receptor (RyR) Ca(2+) release channel mobilizes Ca(2+) from internal stores to support a variety of cellular functions, including the inflammatory response after ischemia and reperfusion. The

Role of the ryanodine receptor in ischemic brain damage--localized reduction of ryanodine receptor binding during ischemia in hippocampus CA1.

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1. The ryanodine receptor has recently been shown to play a pivotal role in the regulation of intracellular Ca2+ concentration via Ca(2+)-induced Ca2+ release (CICR). Effects of ischemia on CICR in the brain tissue, however, remain largely unknown since only a few reports have been published on this

cADP-ribose/ryanodine channel/Ca2+-release signal transduction pathway in mesangial cells.

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Signaling via release of Ca2+ from intracellular stores is mediated by several systems, including the inositol 1,4,5-trisphosphate (IP3) and cADP-ribose (cADPR) pathway. We recently discovered a high capacity for cADPR synthesis in rat glomeruli and cultured mesangial cells (MC). We sought to

Involvement of calcium and arachidonate metabolism in acetylated-low-density-lipoprotein-stimulated tumor-necrosis-factor-alpha production by rat peritoneal macrophages.

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We show that lipopolysaccharide-free actetylated low-density lipoprotein (LDL), but not native LDL, stimulates tumor-necrosis factor-alpha (TNF-alpha) secretion by rat peritoneal macrophages and the signal-transduction pathways involved. The role of the scavenger receptor (SR) in this response was

Nitric oxide is not involved in the endotoxemia-induced alterations in Ca2+ and ryanodine responses in mouse diaphragms.

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Lipopolysaccharide (LPS, endotoxin)-induced diaphragmatic contractile dysfunction and sarcolemmal injury in animals has been identified. However, the precise nature of sepsis-related alterations in diaphragm myofiber function and the activity of Ca(2+) release from sarcoplasmic reticulum of skeletal

Ca2+ mediates axotomy-induced necrosis and apoptosis of satellite glial cells remote from the transection site in the isolated crayfish mechanoreceptor.

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Severe nerve injury such as axotomy induces neuron degeneration and death of surrounding glial cells. Using a crayfish stretch receptor that consists of a single mechanoreceptor neuron enveloped by satellite glia, we showed that axotomy not only mechanically injures glial cells at the transection

Developmental dependence, the role of the kinases p38 MAPK and PKC, and the involvement of tumor necrosis factor-R1 in the induction of mGlu-5 LTD in the dentate gyrus.

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The mechanisms of mGluR-LTD were studied in the dentate gyrus in vitro. The most effective protocol for inducing mGluR-LTD in 6-8 week animals was brief high frequency stimulation (HFS) applied in the presence of the NMDAR antagonist AP5. Evidence for HFS inducing LTD via activation of

Tumor necrosis factor (TNF) modulates synaptic plasticity in a concentration-dependent manner through intracellular calcium stores.

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The role of inflammatory signaling pathways in synaptic plasticity has long been identified. Yet, it remains unclear how inflammatory cytokines assert their pleiotropic effects on neural plasticity. Moreover, the neuronal targets through which inflammatory cytokines assert their effects on

The signalling pathway of CaMKII-mediated apoptosis and necrosis in the ischemia/reperfusion injury.

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Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) plays an important role mediating apoptosis/necrosis during ischemia-reperfusion (IR). We explored the mechanisms of this deleterious effect. Langendorff perfused rat and transgenic mice hearts with CaMKII inhibition targeted to sarcoplasmic

TNF Induces Pathogenic Programmed Macrophage Necrosis in Tuberculosis through a Mitochondrial-Lysosomal-Endoplasmic Reticulum Circuit.

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Necrosis of infected macrophages constitutes a critical pathogenetic event in tuberculosis by releasing mycobacteria into the growth-permissive extracellular environment. In zebrafish infected with Mycobacterium marinum or Mycobacterium tuberculosis, excess tumor necrosis factor triggers programmed

Neferine induces autophagy-dependent cell death in apoptosis-resistant cancers via ryanodine receptor and Ca2+-dependent mechanism.

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Resistance of cancer cells to chemotherapy is a significant clinical concern and mechanisms regulating cell death in cancer therapy, including apoptosis, autophagy or necrosis, have been extensively investigated over the last decade. Accordingly, the identification of medicinal compounds against

Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids.

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The early proinflammatory cytokine tumor necrosis factor (TNF) is released in significant quantities by the activated immune system in response to infection, leukemia, autoimmune disorders, and radiation sickness. Nausea, emesis, and anorexia are common features of these disorders. TNF action on

Evidence for a role for the group I metabotropic glutamate receptor in the inhibitory effect of tumor necrosis factor-alpha on long-term potentiation.

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Pro-inflammatory cytokines are known to be elevated in several neuropathological states that are associated with learning and memory. We have previously demonstrated in our laboratory that the inhibition of long-term potentiation (LTP) in the dentate gyrus region of the rat hippocampus, by tumor

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