β-amyloid inhibition of long-term potentiation is mediated via tumor necrosis factor
| العنوان: | β-amyloid inhibition of long-term potentiation is mediated via tumor necrosis factor |
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| المؤلفون: | Qinwen Wang, Michael J. Rowan, Roger Anwyl, Jinqun Wu |
| المصدر: | European Journal of Neuroscience. 22:2827-2832 |
| بيانات النشر: | Wiley, 2005. |
| سنة النشر: | 2005 |
| مصطلحات موضوعية: | Male, p38 mitogen-activated protein kinases, medicine.medical_treatment, Long-Term Potentiation, In Vitro Techniques, Biology, Pharmacology, Membrane Potentials, Mice, medicine, LTP induction, Animals, Receptor, Mice, Knockout, Amyloid beta-Peptides, Tumor Necrosis Factor-alpha, musculoskeletal, neural, and ocular physiology, General Neuroscience, Antagonist, Long-term potentiation, Electric Stimulation, Rats, Electrophysiology, Mice, Inbred C57BL, Cytokine, nervous system, Receptors, Tumor Necrosis Factor, Type I, Mitogen-activated protein kinase, Immunology, biology.protein, Tumor necrosis factor alpha |
| الوصف: | A number of recent studies have shown that beta-amyloid (Abeta) inhibits the induction of long-term potentiation (LTP) in the hippocampus. However, little is known about the mechanisms underlying such inhibition of LTP. In the present study, we present evidence that the cytokine tumor necrosis factor (TNF) alpha has a key role in the Abeta inhibition of LTP. The suppression of LTP by Abeta was absent in mutant mice null for TNF receptor type 1 (TNF-R1) and was prevented by the inhibitors of TNFalpha, infliximab and TNF peptide antagonist, and by the inhibitor of TNFalpha production, thalidomide. In addition, exogenous TNFalpha inhibited LTP induction, an action mediated via TNF-R1 as such inhibition was absent in mutant mice null for TNF-R1. The inhibition of LTP by TNFalpha involved activation of group I metabotropic glutamate receptor and p38 MAP kinase, identical to that for the Abeta-mediated inhibition of LTP induction. |
| تدمد: | 1460-9568 0953-816X |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f36ce5ab1e900cca0f5826c61131e871 https://doi.org/10.1111/j.1460-9568.2005.04457.x |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi.dedup.....f36ce5ab1e900cca0f5826c61131e871 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14609568 0953816X |
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