WordNet
- a thin pliable sheet of material
- a pliable sheet of tissue that covers or lines or connects the organs or cells of animals or plants (同)tissue layer
PrepTutorEJDIC
- (生物の)膜,皮膜
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- 1. 赤血球細胞膜の動態および機構 red blood cell membrane dynamics and organization
- 2. 血液-血液透析膜の相互作用に関与する生化学的機序 biochemical mechanisms involved in blood hemodialysis membrane interactions
- 3. ライソゾーム膜蛋白質2欠損症（糖原病IIb型、ダノン病） lysosome associated membrane protein 2 deficiency glycogen storage disease iib danon disease
- 4. 血液透析膜の生体適合性についての臨床結果 clinical consequences of hemodialysis membrane biocompatibility
- 5. 補体系の制御因子および受容体 regulators and receptors of the complement system
English Journal
- Selective inhibition of caspases in skeletal muscle reverses the apoptotic synaptic degeneration in slow-channel myasthenic syndrome.
- Zhu H1, Pytel P, Gomez CM.Author information 1Department of Neurology and.AbstractSlow-channel syndrome (SCS) is a congenital myasthenic disorder caused by point mutations in subunits of skeletal muscle acetylcholine receptor leading to Ca(2+) overload and degeneration of the postsynaptic membrane, nuclei and mitochondria of the neuromuscular junction (NMJ). In both SCS muscle biopsies and transgenic mouse models for SCS (mSCS), the endplate regions are shrunken, and there is evidence of DNA damage in the subsynaptic region. Activated caspase-9, -3 and -7 are intensely co-localized at the NMJ, and the Ca(2+)-activated protease, calpain, and the atypical cyclin-dependent kinase (Cdk5) are overactivated in mSCS. Thus, the true mediator(s) of the disease process is not clear. Here, we demonstrate that selective inhibition of effector caspases, caspase-3 and -7, or initiator caspase, caspase-9, in limb muscle in vivo by localized expression of recombinant inhibitor proteins dramatically decreases subsynaptic DNA damage, increases endplate area and improves ultrastructural abnormalities in SCS transgenic mice. Calpain and Cdk5 are not affected by this treatment. On the other hand, inhibition of Cdk5 by expression of a dominant-negative form of Cdk5 has no effect on the degeneration. Together with previous studies, these results indicate that focal activation of caspase activity at the NMJ is the principal pathological process responsible for the synaptic apoptosis in SCS. Thus, treatments that reduce muscle caspase activity are likely to be of benefit for SCS patients.
- Human molecular genetics.Hum Mol Genet.2014 Jan 1;23(1):69-77. doi: 10.1093/hmg/ddt397. Epub 2013 Aug 13.
- Slow-channel syndrome (SCS) is a congenital myasthenic disorder caused by point mutations in subunits of skeletal muscle acetylcholine receptor leading to Ca(2+) overload and degeneration of the postsynaptic membrane, nuclei and mitochondria of the neuromuscular junction (NMJ). In both SCS muscle bi
- PMID 23943790
- Confocal imaging of fluorescently labeled proteins in the Drosophila larval neuromuscular junction.
- Coyle IP.Author information IP Coyle Intellectual Property Agency, Fort Lauderdale, FL, USA.AbstractThe Drosophila larval neuromuscular junction (NMJ) consists of a presynaptic motor neuron terminal and a postsynaptic muscle cell that offer an accessible and popular model system for the analysis of synaptic growth and function. I describe techniques for visualizing fluorescently labeled proteins within dissected, formaldehyde-fixed second to third instar larval NMJs. In addition, I present two strategies using confocal microscopy to solve a particular problem in NMJ analysis: distinguishing fluorescence in the presynaptic nerve terminal from that in the adjacent postsynaptic muscle cell. This problem arises from the fact that the membrane of the muscle cell envelops the motor neuron terminal with a convoluted process called the subsynaptic reticulum, obscuring the boundary between muscle and nerve. A first strategy entails taking thin optical sections through synaptic boutons to capture a cross section of the nerve terminal, and a second strategy involves visualizing epitope-tagged isoforms of particular proteins that have been transgenically expressed in either the nerve or the muscle.
- Methods in molecular biology (Clifton, N.J.).Methods Mol Biol.2014;1075:201-12. doi: 10.1007/978-1-60761-847-8_9.
- The Drosophila larval neuromuscular junction (NMJ) consists of a presynaptic motor neuron terminal and a postsynaptic muscle cell that offer an accessible and popular model system for the analysis of synaptic growth and function. I describe techniques for visualizing fluorescently labeled proteins w
- PMID 24052353
- Subunit composition and kinetics of the Renshaw cell heteromeric nicotinic receptors.
- Lamotte d'Incamps B1, Ascher P.Author information 1Neurophysique et Physiologie, CNRS UMR 8119, Université Paris Descartes, France.AbstractIn Renshaw cells (RCs) of newborn mice, activation of motoneurons elicits a four-component synaptic current (EPSC) mediated by two glutamate receptors and two nicotinic receptors (nAChRs). We have analyzed the nicotinic component of the EPSC which is blocked by dihydro-beta-erythroidine (DHβE) with the dual objective of identifying the nAChR subunits involved and of understanding the kinetics of the response. The sensitivity to DHβE of the peak of the EPSC was differentially affected by genetic deletion of three specific nAChR subunits: α2, β2 and β4. The comparison of these effects with published findings on recombinant receptors suggests that, in WT mice, two heteromeric assemblies, α4β2 and α2β4, coexist in variable proportions in a given RC. Some results seem to require, however, the involvement of an additional subunit. The effects of DHβE on the decay of the EPSCs were compared in WT mice and in PRiMA(-/-) mice, in which the decay is prolonged by the absence of central acetylcholinesterase. In PRiMA(-/-) mice DHβE shortened the decay of the EPSC. In WT mice it did not alter the decay but reduced the amplitude of both components of the EPSC. The results can be interpreted by assuming that the nAChRs exist in two stoichiometries, subsynaptic "low sensitivity" nAChRs and extrasynaptic "high sensitivity" nAChRs activated by spillover.
- Biochemical pharmacology.Biochem Pharmacol.2013 Oct 15;86(8):1114-21. doi: 10.1016/j.bcp.2013.06.017. Epub 2013 Jun 26.
- In Renshaw cells (RCs) of newborn mice, activation of motoneurons elicits a four-component synaptic current (EPSC) mediated by two glutamate receptors and two nicotinic receptors (nAChRs). We have analyzed the nicotinic component of the EPSC which is blocked by dihydro-beta-erythroidine (DHβE) with
- PMID 23811311
Japanese Journal
- Interaction between gustatory depolarizing receptor potential and efferent-induced slow depolarizing synaptic potential in frog taste cell.
- Cellular and molecular neurobiology 29(2), 243-252, 2009-03
- NAID 120001629879
- Electron spectroscopic imaging (ESI) of cobalt ions responsible for the blockade of synaptic transmission and excitability of muscle cells in frog neuromuscular preparations
- Proceedings of the Japan Academy, Series B 76(1), 7-11, 2000
- NAID 130000903772
- Hyperpolarization Caused by External High Potassium in Snail Neurons
- The Japanese Journal of Physiology 28(3), 249-263, 1978
- NAID 130003476671
Related Links
- PDF | We here describe the methodology to carry out a fractionation procedure that separates presynaptic, postsynaptic, and extrasynaptic fraction, allowing to access the localization of proteins within synapses, which ...
- Assembly and Turnover of the Subsynaptic Membrane H. Betz and H. Rehm 1 Introduction Synapses are the basic structural elements for information transfer bet ween excitable cells in the nervous system, and their properties ...
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| リンク元 | 「シナプス後膜」「シナプス下膜」 |
| 関連記事 | 「membrane」 |
「シナプス後膜」
- シナプス後ニューロンの細胞膜
「シナプス下膜」
「membrane」
- n.