WordNet
- the gears that transmit power from an automobile engine via the driveshaft to the live axle (同)transmission system
- the act of sending a message; causing a message to be transmitted (同)transmittal, transmitting
- communication by means of transmitted signals
- (neuroscience) of or involving synapses
PrepTutorEJDIC
- (また transmittal)〈U〉(…を)伝える(送る)こと,(…が)伝えられる(送られる)こし,(…の)伝達,伝送《+of+名》 / 〈C〉(ラジオ・テレビなどで)送られたもの(画面・番組など) / 〈C〉伝動装置,(車の)変速装置,ギヤ
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- 1. B型肝炎ウイルス感染の疫学、伝染、および予防 epidemiology transmission and prevention of hepatitis b virus infection
- 2. 資源の限られた状況におけるHIVの母子感染の予防 prevention of mother to child hiv transmission in resource limited settings
- 3. 痙攣発作およびてんかんの病態生理 pathophysiology of seizures and epilepsy
- 4. ヒトヘルペスウイルス8感染のウイルス学、疫学、および伝播 virology epidemiology and transmission of human herpesvirus 8 infection
- 5. 麻疹の疫学および伝染 epidemiology and transmission of measles
English Journal
- The Discovery of Human of GLUD2 Glutamate Dehydrogenase and Its Implications for Cell Function in Health and Disease.
- Shashidharan P, Plaitakis A.Author information Department of Neurology, Icahn School of Medicine at Mount Sinai, Box 1137, One Gustave L Levy Place, New York, NY, 10029, USA, pullani.shashi@mssm.edu.AbstractWhile the evolutionary changes that led to traits unique to humans remain unclear, there is increasing evidence that enrichment of the human genome through DNA duplication processes may have contributed to traits such as bipedal locomotion, higher cognitive abilities and language. Among the genes that arose through duplication in primates during the period of increased brain development was GLUD2, which encodes the hGDH2 isoform of glutamate dehydrogenase expressed in neural and other tissues. Glutamate dehydrogenase GDH is an enzyme central to the metabolism of glutamate, the main excitatory neurotransmitter in mammalian brain involved in a multitude of CNS functions, including cognitive processes. In nerve tissue GDH is expressed in astrocytes that wrap excitatory synapses, where it is thought to play a role in the metabolic fate of glutamate removed from the synaptic cleft during excitatory transmission. Expression of GDH rises sharply during postnatal brain development, coinciding with nerve terminal sprouting and synaptogenesis. Compared to the original hGDH1 (encoded by the GLUD1 gene), which is potently inhibited by GTP generated by the Krebs cycle, hGDH2 can function independently of this energy switch. In addition, hGDH2 can operate efficiently in the relatively acidic environment that prevails in astrocytes following glutamate uptake. This adaptation is thought to provide a biological advantage by enabling enhanced enzyme catalysis under intense excitatory neurotransmission. While the novel protein may help astrocytes to handle increased loads of transmitter glutamate, dissociation of hGDH2 from GTP control may render humans vulnerable to deregulation of this enzyme's function. Here we will retrace the cloning and characterization of the novel GLUD2 gene and the potential implications of this discovery in the understanding of mechanisms that permitted the brain and other organs that express hGDH2 to fine-tune their functions in order to meet new challenging demands. In addition, the potential role of gain-of-function of hGDH2 variants in human neurodegenerative processes will be considered.
- Neurochemical research.Neurochem Res.2014 Mar;39(3):460-70. doi: 10.1007/s11064-013-1227-5. Epub 2013 Dec 19.
- While the evolutionary changes that led to traits unique to humans remain unclear, there is increasing evidence that enrichment of the human genome through DNA duplication processes may have contributed to traits such as bipedal locomotion, higher cognitive abilities and language. Among the genes th
- PMID 24352816
- Tuning into diversity of homeostatic synaptic plasticity.
- Lee KF1, Soares C1, Béïque JC2.Author information 1Neuroscience Graduate Program, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada; Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.2Centre for Stroke Recovery, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada; Centre for Neural Dynamics, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada; Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada. Electronic address: jbeique@uottawa.ca.AbstractNeurons are endowed with the remarkable ability to integrate activity levels over time and tune their excitability such that action potential firing is maintained within a computationally optimal range. These feedback mechanisms, collectively referred to as "homeostatic plasticity", enable neurons to respond and adapt to prolonged alterations in neuronal activity by regulating several determinants of cellular excitability. Perhaps the best-characterized of these homeostatic responses involves the regulation of excitatory glutamatergic transmission. This homeostatic synaptic plasticity (HSP) operates bidirectionally, thus providing a means for neurons to tune cellular excitability in response to either elevations or reductions in net activity. The last decade has seen rapid growth in interest and efforts to understand the mechanistic underpinnings of HSP in part because of the theoretical stabilization that HSP confers to neural network function. Since the initial reports describing HSP in central neurons, innovations in experimental approaches have permitted the mechanistic dissection of this cellular adaptive response and, as a result, key advances have been made in our understanding of the cellular and molecular basis of HSP. Here, we review recent evidence that outline the presence of distinct forms of HSP at excitatory glutamatergic synapses which operate at different sub-cellular levels. We further present theoretical considerations on the potential computational roles afforded by local, synapse-specific homeostatic regulation. This article is part of the Special Issue entitled 'Homeostatic Synaptic Plasticity'.
- Neuropharmacology.Neuropharmacology.2014 Mar;78:31-7. doi: 10.1016/j.neuropharm.2013.03.016. Epub 2013 Mar 27.
- Neurons are endowed with the remarkable ability to integrate activity levels over time and tune their excitability such that action potential firing is maintained within a computationally optimal range. These feedback mechanisms, collectively referred to as "homeostatic plasticity", enable neurons t
- PMID 23541721
- CaMKII Activity in the Ventral Tegmental Area Gates Cocaine-Induced Synaptic Plasticity in the Nucleus Accumbens.
- Liu X1, Liu Y2, Zhong P2, Wilkinson B2, Qi J3, Olsen CM4, Bayer KU5, Liu QS4.Author information 11] Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA [2] Department of Physiology, Shanxi Medical University, Taiyuan, China.2Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA.3Department of Physiology, Shanxi Medical University, Taiyuan, China.41] Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA [2] Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI, USA.5Department of Pharmacology, University of Colorado Denver, Aurora, CO, USA.AbstractAddictive drugs such as cocaine induce synaptic plasticity in discrete regions of the reward circuit. The aim of the present study is to investigate whether cocaine-evoked synaptic plasticity in the ventral tegmental area (VTA) and nucleus accumbens (NAc) is causally linked. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a central regulator of long-term synaptic plasticity, learning, and drug addiction. We examined whether blocking CaMKII activity in the VTA affected cocaine conditioned place preference (CPP) and cocaine-evoked synaptic plasticity in its target brain region, the NAc. TatCN21 is a CaMKII inhibitory peptide that blocks both stimulated and autonomous CaMKII activity with high selectivity. We report that intra-VTA microinjections of tatCN21 before cocaine conditioning blocked the acquisition of cocaine CPP, whereas intra-VTA microinjections of tatCN21 before saline conditioning did not significantly affect cocaine CPP, suggesting that the CaMKII inhibitor blocks cocaine CPP through selective disruption of cocaine-cue-associated learning. Intra-VTA tatCN21 before cocaine conditioning blocked cocaine-evoked depression of excitatory synaptic transmission in the shell of the NAc slices ex vivo. In contrast, intra-VTA microinjection of tatCN21 just before the CPP test did not affect the expression of cocaine CPP and cocaine-induced synaptic plasticity in the NAc shell. These results suggest that CaMKII activity in the VTA governs cocaine-evoked synaptic plasticity in the NAc during the time window of cocaine conditioning.
- Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology.Neuropsychopharmacology.2014 Mar;39(4):989-99. doi: 10.1038/npp.2013.299. Epub 2013 Oct 24.
- Addictive drugs such as cocaine induce synaptic plasticity in discrete regions of the reward circuit. The aim of the present study is to investigate whether cocaine-evoked synaptic plasticity in the ventral tegmental area (VTA) and nucleus accumbens (NAc) is causally linked. Ca(2+)/calmodulin-depend
- PMID 24154664
Japanese Journal
- A 型ボツリヌス毒素は神経障害性疼痛による脊髄興奮性シナプスの増強を抑制する
- 根本 興平
- Dokkyo journal of medical sciences 41(1), 71-78, 2014-03-25
- A 型ボツリヌス毒素(BoNT/A)の神経障害性疼痛に対する鎮痛機序を明らかにするために,マウスの坐骨神経部分結紮モデルの髄腔内にBoNT/A を投与し,BoNT/A がvon-Frey 試験による痛み回避行動への作用とパッチクランプ・ホールセル記録法による脊髄後角興奮性シナプス伝達に及ぼす作用を評価した.坐骨神経の部分結紮後に0.15 単位のBoNT/A を髄腔内投与し,von-Frey 試験に …
- NAID 110009783347
- Regulation and functional roles of rebound potentiation at cerebellar stellate cell—Purkinje cell synapses
- Hirano Tomoo,Kawaguchi Shin-ya
- Frontiers in Cellular Neuroscience 8, 2014-02-18
- … Purkinje cells receive both excitatory and inhibitory synaptic inputs and send sole output from the cerebellar cortex. … Long-term depression (LTD), a type of synaptic plasticity, at excitatory parallel fiber–Purkinje cell synapses has been studied extensively as a primary cellular mechanism of motor learning. …
- NAID 120005385884
- 電気生理学的手法を用いた慢性疼痛の病態解明と薬理学的評価
- 田辺 光男
- YAKUGAKU ZASSHI 134(3), 405-412, 2014
- … To characterize these pathophysiological changes and pharmacological properties in chronic pain conditions at the synaptic level, we have employed in vitro electrophysiology in slices of the spinal cord and supraspinal regions such as brainstem and hippocampus of adult mice and in vivo electrophysiology in anesthetized rats. …
- NAID 130003391183
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| 関連記事 | 「transmission」「excitatory」「synaptic」「synaptic transmission」 |
「transmission」
- n.
- 関
- communication、contagion、convey、infect、infection、infestation、penetrate、penetration、permeate、transduce、transduction、transductional、transfer、transmit
「excitatory」
- 興奮性の、興奮の
「synaptic」
- シナプスの、シナプス性の
「synaptic transmission」
- 関
- Neurotransmis- sion; Neurotransmitter(s)