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==Articles== | |||
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[[Category:Malinow]] | {{Article|Honkura, Matsuzaki, Noguchi, Ellis-Davies, Kasai|2008|Cell • [http://www.sciencedirect.com/science/article/pii/S0896627308000743 FullText]|18341992|The subspine organization of actin fibers regulates the structure and plasticity of dendritic spines.}} | ||
<mediaplayer image='http://www.bradleymonk.com/w/images/d/da/Kasai_GluUncaging_S7.png' width='500' height='300'>http://www.bradleymonk.com/w/images/1/18/Kasai_GluUncaging_S7.mov</mediaplayer> | |||
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Two-photon imaging of the confinement of PAGFP-actin fluorescence after repetitive photoactivation and uncaging of MNI-glutamate (60 pulses of 0.6 ms duration at 1 Hz) at a point (square) distal to the apex of the spine shown in Figure 5D. The 2D images were acquired every 10 s for 7 min. Photoactivation was induced at the moment when the white square turns red. Scale bar, 1 μm. </div></html>||<big>SI video1 </big>}} | |||
<mediaplayer image='http://www.bradleymonk.com/w/images/0/06/Kasai_GluUncaging_S8.png' width='500' height='300'>http://www.bradleymonk.com/w/images/6/64/Kasai_GluUncagingLat_S8.mov</mediaplayer> | |||
{{Pop3|[[File:Dot.png]]|<html><video src="http://www.bradleymonk.com/w/images/6/64/Kasai_GluUncagingLat_S8.mov" controls></video> <br> <div style='color:white; width:400px'> Movie S8. | |||
Two-photon imaging of PAGFP-actin fluorescence after repetitive photoactivation and uncaging of MNI-glutamate (60 pulses of 0.6 ms duration at 1 Hz) at a point (square) distal to the apex of the spine shown in Figure 5G in the presence of Lat A (0.1 μM). The 2D images were acquired every 15 s for 10 min. Photoactivation was induced at the moment when the white square turns red. Scale bar, 1 μm. </div></html>||<big>SI video1 </big>}} | |||
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{{Ref|Ehrlich Malinow|14749436}} | |||
[[Category:Malinow]][[Category:Journals]] [[Category:Synaptic Plasticity]] | |||
Revision as of 17:23, 20 March 2015
Lu, Gray, Granger, During, Nicoll • 2011 • J Neurophysiol - PDF
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We thus tested whether GluA2 is required for the potentiation of AMPAR EPSCs following the loss of NMDARs. In the GRIA2fl/fl mice, deleting GluA2 caused about a 50% reduction in the AMPAR EPSC FIG: {{#info: 
{{{2}}} CLICK AWAY FROM IMAGE TO CLOSE }} with no change in the glutamate-evoked AMPAR-mediated outside-out patch currents (B ). Interestingly, in GRIA2fl/flGRIN1fl/fl mice the loss of NMDARs failed to enhance AMPAR EPSCs. In fact, there was a significant further decrease FIG: {{#info: {{{2}}} CLICK AWAY FROM IMAGE TO CLOSE }}. Neither genetic manipulation changes the PPR. In addition, as expected, deletion of GluA2 caused strong inward rectification. Finally, no difference was found in glutamate evoked AMPAR-mediated currents in outside-out patches FIG: {{#info: {{{2}}} CLICK AWAY FROM IMAGE TO CLOSE }}. Therefore in contrast to GluA1, the GluA2 subunit is critical for synaptic potentiation of AMPARs following NMDAR deletion.
Articles
Honkura, Matsuzaki, Noguchi, Ellis-Davies, Kasai • 2008 • Cell • FullText
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