LTP

出典: meddic

長期増強 long-term potentiation

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/08/31 19:32:28」(JST)

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英文文献

  • The effects of a reminder of underwater trauma on behaviour and memory-related mechanisms in the rat dentate gyrus.
  • Ardi Z1, Ritov G1, Lucas M2, Richter-Levin G1.Author information 1Department of Psychology, University of Haifa, Haifa 31905, Israel.2The Institute for the Study of Affective Neuroscience, University of Haifa, 31905 Haifa, Israel.AbstractIntrusive re-experiencing is a core symptom in post-traumatic stress disorder (PTSD), often triggered by contextual cues associated with the trauma. It is not yet clear if intrusive re-experiencing is only the result, or whether it may contribute to the establishment of PTSD following acute stress. This study aimed at examining the impact of an underwater trauma (UWT) reminder on anxiety-like behaviour and on neuronal activity and plasticity in the hippocampus and the amygdala. Sprague-Dawley rats were exposed to UWT and 24 h later were re-exposed to the context. The effects on behaviour, activation of the amygdala (BLA) and dentate gyrus (DG), and on long-term potentiation (LTP) and local circuit activity (frequency-dependent inhibition (FDI) and paired-pulse inhibition (PPI)) in the DG were assessed. The exposure to UWT by itself resulted in increased anxiety behaviour in the open field, together with increased PPI. Upon exposure to the UWT reminder, an additional increase in anxiety was also observed in the EPM and in FDI. Moreover, reminder exposure resulted in impaired DG LTP and a significant BLA extracellular-signal-regulated kinases (ERK) 2 activation. In conclusion, these observed effects of exposure to a trauma reminder, following the exposure to the initial trauma, might be associated with the progression of trauma-related pathologies and the development of related disorders.
  • The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP).Int J Neuropsychopharmacol.2014 Apr;17(4):571-80. doi: 10.1017/S1461145713001272.
  • Intrusive re-experiencing is a core symptom in post-traumatic stress disorder (PTSD), often triggered by contextual cues associated with the trauma. It is not yet clear if intrusive re-experiencing is only the result, or whether it may contribute to the establishment of PTSD following acute stress.
  • PMID 24565178
  • Protective effect of pranlukast on Aβ 1-42-induced cognitive deficits associated with downregulation of cysteinyl leukotriene receptor 1.
  • Tang SS1, Ji MJ1, Chen L1, Hu M1, Long Y1, Li YQ1, Miao MX1, Li JC1, Li N2, Ji H1, Chen XJ2, Hong H1.Author information 1Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China.2Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.AbstractDeposition of extracellular amyloid-β (Aβ) peptide is one of the pathological hallmarks of Alzheimer's disease (AD). Accumulation of Aβ is thought to associate with cognition deficits, neuroinflammation and apoptosis observed in AD. However, effective neuroprotective approaches against Aβ neurotoxicity are unavailable. In the present study, we analysed the effects of pranlukast, a selective cysteinyl leukotriene receptor 1 (CysLT1R) antagonist, on the impairment of learning and memory formation induced by Aβ and the probable underlying electrophysiological and molecular mechanisms. We found that bilateral intrahippocampal injection of Aβ 1-42 resulted in a significant decline of spatial learning and memory of mice in the Morris water maze (MWM) and Y-maze tests, together with a serious depression of in vivo hippocampal long-term potentiation (LTP) in the CA1 region of the mice. Importantly, this treatment caused significant increases in CysLT1R expression and subsequent NF-κB signaling, caspase-3 activation and Bcl-2 downregulation in the hippocampus or prefrontal cortex. Oral administration of pranlukast at 0.4 or 0.8 mg/kg for 4 wk significantly reversed Aβ 1-42-induced impairments of cognitive function and hippocampal LTP in mice. Furthermore, pranlukast reversed Aβ 1-42-induced CysLT1R upregulation, and markedly suppressed the Aβ 1-42-triggered NF-κB pathway, caspase-3 activation and Bcl-2 downregulation in the hippocampus and prefrontal cortex in mice. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay confirmed its presence in the brain after oral administration of pranlukast in mice. These data disclose novel findings about the therapeutic potential of pranlukast, revealing a previously unknown therapeutic possibility to treat memory deficits associated with AD.
  • The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP).Int J Neuropsychopharmacol.2014 Apr;17(4):581-92. doi: 10.1017/S1461145713001314. Epub 2013 Nov 11.
  • Deposition of extracellular amyloid-β (Aβ) peptide is one of the pathological hallmarks of Alzheimer's disease (AD). Accumulation of Aβ is thought to associate with cognition deficits, neuroinflammation and apoptosis observed in AD. However, effective neuroprotective approaches against Aβ neurot
  • PMID 24229499
  • Glucagon-like peptide-1 protects synaptic and learning functions from neuroinflammation in rodents.
  • Iwai T1, Sawabe T, Tanimitsu K, Suzuki M, Sasaki-Hamada S, Oka J.Author information 1Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba, Japan.AbstractGlucagon-like peptide-1 (GLP-1) is derived from the processing of proglucagon in intestinal L-cells and releases insulin from pancreatic β-cells as an incretin. The GLP-1 receptor has been proposed as a possible therapeutic target for the treatment of Alzheimer's disease, in which neuroinflammation is critical in the pathogenesis. The present study investigates whether GLP-1 (7-36) amide, an active fragment of GLP-1, protected against synaptic impairments induced by inflammation-related injurious agents (lipopolysaccharide [LPS], interleukin-1β [IL-1β], and H2 O2 ). In the Y-maze test, LPS (10 μg/mouse, i.c.v) significantly decreased the percentage alternation. Pretreatment with GLP-1 (7-36) amide (0.09-0.9 nmol/mouse, i.c.v.) prevented an impairment in spontaneous alternation performance. Pretreatment with LPS (10 μg/ml, 2 hr) impaired LTP induction but not paired-pulse facilitation in the CA1 region of rat hippocampal slices. This impairment was prevented by cotreatment with GLP-1 (7-36) amide (50 nM). IL-1β (0.57 nM) or H2 O2 (50 μM) also impaired LTP induction. This impairment was prevented by GLP-1 (7-36) amide (50 nM). These results suggest that GLP-1 (7-36) amide improves the synaptic impairments induced by inflammation-related injurious agents in the CA1 region of the hippocampus. © 2014 Wiley Periodicals, Inc.
  • Journal of neuroscience research.J Neurosci Res.2014 Apr;92(4):446-54. doi: 10.1002/jnr.23335. Epub 2014 Jan 27.
  • Glucagon-like peptide-1 (GLP-1) is derived from the processing of proglucagon in intestinal L-cells and releases insulin from pancreatic β-cells as an incretin. The GLP-1 receptor has been proposed as a possible therapeutic target for the treatment of Alzheimer's disease, in which neuroinflammation
  • PMID 24464856

和文文献

  • 脳梗塞後の機能回復 : 脳梗塞モデルとリハビリテーション(再生医療の進歩,2012年,第53回日本心身医学会総会ならびに学術講演会(鹿児島))
  • 池田 聡
  • 心身医学 53(8), 742-747, 2013-08-01
  • … 容器の障害に照応し,脳の機能局在やネットワークを変化させることができることが解明されてきた.そのメカニズムは既存の使用されていなかった回路の使用(unmasking),シナプス伝達の効率増強(long term potentiation:LTP),シナプス伝達の効率抑制(long term depression:LTD),引き続いて起こるシナプスの形態変化,樹状突起・軸索の側芽延長,シナプス新生,ひいては神経幹細胞からの神経細胞新生までさまざまな機構があることがわかっ …
  • NAID 110009624738
  • 北東アジアの地域協力に対する新たな視座 : 酸性雨問題をめぐるレジーム・コンプレックス
  • 横田 将志
  • 北東アジア地域研究 (19), 97-108, 2013-06-30
  • … And, three regional frameworks were built: (1) EANET (Acid Deposition Monitoring Network in East Asia), (2) NEASPEC (North-East Asian Subregional Programme for Environmental Cooperation, (3) LTP (Joint Research Project on Long-Range Transboundary Air Pollutants in Northeast Asia). … EANET, NEASPEC and LTP are partially overlapping without any agreed hierarchy and coordinator for resolving the overlap. …
  • NAID 110009630598
  • Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats
  • Zhang Lifeng,Jin Cuihong,Liu Qiufang [他]
  • The Journal of toxicological sciences : an official journal of the Japanese Society of Toxicology 38(2), 255-268, 2013-04
  • NAID 40019678622

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関連画像

Image:model_for_the_induciton_of_LTP.JPGltp Cork City Council to reduce Local Long Term Potentiation (LTP)ltp Cork City Council to reduce Local 細胞外シグナル制御キナーゼ File:LTP exemplar.jpg - Wikimedia Commons


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リンク元長期増強」「シナプス後仮説」「シナプス前仮説
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関連記事L」「LT

長期増強」

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long-term potentiation LTP
  • 海馬や大脳皮質のシナプスではテタヌス刺激後、シナプス後電位の振幅の増大が数時間以上持続する。この現象を長期増強と呼ぶ。SP:168




シナプス後仮説」

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LTPシナプス前仮説シナプス後仮説


シナプス前仮説」

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LTPシナプス前仮説シナプス後仮説


PLTP」

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Phospholipid transfer protein


L」

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WordNet   license wordnet

「the 12th letter of the Roman alphabet」
l

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「lira(イタリアの貨幣単位リラ)」


LT」

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