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1
المؤلفون: Erin D. Milligan, Kristin K. Mehmert, Steven F. Maier, Justin L. Hinde, Linda R. Watkins, Lewis O. Harvey, Kevin J. Tracey, David Martin
المصدر: Brain research. 861(1)
مصطلحات موضوعية: Male, Hot Temperature, HIV Envelope Protein gp120, Rats, Sprague-Dawley, Immune system, medicine, Nociception assay, Animals, Citrates, Molecular Biology, Microglia, business.industry, General Neuroscience, Anti-Inflammatory Agents, Non-Steroidal, Hydrazones, Spinal cord, nervous system diseases, Rats, Specific Pathogen-Free Organisms, Allodynia, medicine.anatomical_structure, Spinal Cord, Hyperalgesia, Touch, Immunology, Neurology (clinical), medicine.symptom, business, Neuroscience, Neuroglia, Tail flick test, Developmental Biology, Astrocyte
الوصف: Astrocytes and microglia in the spinal cord have recently been reported to contribute to the development of peripheral inflammation-induced exaggerated pain states. Both lowering of thermal pain threshold (thermal hyperalgesia) and lowering of response threshold to light tactile stimuli (mechanical allodynia) have been reported. The notion that spinal cord glia are potential mediators of such effects is based on the disruption of these exaggerated pain states by drugs thought to preferentially affect glial function. Activation of astrocytes and microglia can release many of the same substances that are known to mediate thermal hyperalgesia and mechanical allodynia. The aim of the present series of studies was to determine whether exaggerated pain states could also be created in rats by direct, intraspinal immune activation of astrocytes and microglia. The immune stimulus used was peri-spinal (intrathecal, i.t.) application of the Human Immunodeficiency Virus type 1 (HIV-1) envelope glycoprotein, gp120. This portion of HIV-1 is known to bind to and activate microglia and astrocytes. Robust thermal hyperalgesia (tail-flick, TF, and Hargreaves tests) and mechanical allodynia (von Frey and touch-evoked agitation tests) were observed in response to i.t. gp120. Heat denaturing of the complex protein structure of gp120 blocked gp120-induced thermal hyperalgesia. Lastly, both thermal hyperalgesia and mechanical allodynia to i.t. gp120 were blocked by spinal pretreatment with drugs (fluorocitrate and CNI-1493) thought to preferentially disrupt glial function.
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2
المؤلفون: John M. Hallenbeck, David Martin, Hiroshi Nawashiro
المصدر: Brain research. 778(2)
مصطلحات موضوعية: Male, TNF binding protein, Sialoglycoproteins, Ischemia, Biotin, Arterial Occlusive Diseases, DNA Fragmentation, Pharmacology, Neuroprotection, Receptors, Tumor Necrosis Factor, Brain Ischemia, Cyclic N-Oxides, Mice, medicine, Animals, cardiovascular diseases, Middle cerebral artery occlusion, Molecular Biology, Neurons, Mice, Inbred BALB C, Staining and Labeling, business.industry, Tumor Necrosis Factor-alpha, General Neuroscience, Receptors, Interleukin-1, Cerebral Infarction, Free Radical Scavengers, medicine.disease, nervous system diseases, Interleukin 1 Receptor Antagonist Protein, Tumor Necrosis Factor Decoy Receptors, Neuroprotective Agents, Receptors, Tumor Necrosis Factor, Type I, Anesthesia, Phosphopyruvate Hydratase, Ischemic stroke, Infarct volume, cardiovascular system, DNA fragmentation, Tumor necrosis factor alpha, Nitrogen Oxides, Neurology (clinical), business, Deoxyuracil Nucleotides, Developmental Biology
الوصف: The effect of tumor necrosis factor binding protein (TNFbp) was studied in mice subjected to a permanent middle cerebral artery occlusion (MCAO). TNFbp is a dimeric form of the type I soluble TNF receptor linked to polyethylene glycol (TNFbp), and binds and inhibits TNF-alpha. TNFbp produced a significant reduction in the cortical infarct volume (22.6 +/- 3.5 mm3 immediately after MCAO; 25.2 +/- 2.4 mm3 1 h after MCAO) compared with vehicle-treated animals (30.3 +/- 3.7 mm3 immediately post MCAO; 31 +/- 3.7 mm3 1 h after MCAO (mean +/- S.D.) when administered intracranially up to 60 min post-occlusion. The neuroprotective effect of TNFbp was sustained in mice for 2 weeks after MCAO. DNA fragmentation at the margin of the cortical infarcts was dramatically reduced in mice treated with TNFbp whereas all control animals showed consistent and obvious DNA fragmentation 2 weeks after MCAO. TNFbp could have therapeutic value for the treatment of ischemic stroke if the problem of delivery to brain can be overcome.
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3
المؤلفون: Toshiho Ohtsuki, Kaoru Tasaki, Hiroshi Nawashiro, John M. Hallenbeck, David Martin, Christl A. Ruetzler
المصدر: Brain research. 748(1-2)
مصطلحات موضوعية: Pre treatment, Lipopolysaccharides, Male, medicine.medical_specialty, Lipopolysaccharide, Ischemia, Receptors, Tumor Necrosis Factor, Brain Ischemia, chemistry.chemical_compound, Internal medicine, Rats, Inbred SHR, medicine, Animals, cardiovascular diseases, Middle cerebral artery occlusion, Molecular Biology, business.industry, General Neuroscience, Cerebral Infarction, medicine.disease, Rats, Tumor Necrosis Factor Decoy Receptors, Endocrinology, chemistry, Receptors, Tumor Necrosis Factor, Type I, Anesthesia, Infarct volume, Hypertension, cardiovascular system, Tumor necrosis factor alpha, Neurology (clinical), business, Carrier Proteins, Developmental Biology
الوصف: Ischemic tolerance was induced in spontaneously hypertensive rats (SHR) by injection of a single dose of lipopolysaccharide (LPS) (0.9 mg/kg, i.v.) 1–7 days prior to permanent middle cerebral artery occlusion (MCAO). Infarct volume, evaluated 24 h after MCAO, was significantly reduced by LPS administration 2, 3 or 4 days prior to MCAO (22.8, 25.9 and 20.5%, respectively). The beneficial effect of LPS pre-treatment was completely nullified by concurrent administration of TNFbp. On this basis, the tolerance to ischemia induced by LPS is likely to be mediated by TNF-α.
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