Nicoll - Revision history

Bradley Monk at 07:07, 21 March 2015

2015-03-21T07:07:55Z

← Older revision		Revision as of 00:07, 21 March 2015
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	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}


	[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|400px]]		[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|400px]]
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	[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|400px]]		[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|400px]]		[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|400px]]

			== Main Findings==

	All WT AMPARs contain GluA2.		All WT AMPARs contain GluA2.
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	Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from WT animals at the age of 2–4 weeks under basal conditions.		Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from WT animals at the age of 2–4 weeks under basal conditions.

	Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to ~~�50~~% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused an 50% loss of AMPAR EPSCs.		Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to 50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused an 50% loss of AMPAR EPSCs.


	== GluR2 DELETION ==		=== GluR2 DELETION ===
	GRIA2(fl/fl)		GRIA2(fl/fl)
	ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE		ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE
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	== GluR1 DELETION ==		=== GluR1 DELETION ===
	GRIA1(fl/fl)		GRIA1(fl/fl)
	ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE		ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE

Bradley Monk at 07:06, 21 March 2015

2015-03-21T07:06:15Z

← Older revision		Revision as of 00:06, 21 March 2015
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	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}

	[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|400px]]

	All WT AMPARs contain GluA2.		All WT AMPARs contain GluA2.

Bradley Monk at 07:05, 21 March 2015

2015-03-21T07:05:11Z

← Older revision		Revision as of 00:05, 21 March 2015
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	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}

			[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|500px]]
			[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|500px]]
			[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|500px]]
			[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|500px]]
			[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|500px]]

	All WT AMPARs contain GluA2.		All WT AMPARs contain GluA2.
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	80% of synaptic AMPARs		80% of synaptic AMPARs

	GluR2/3 receptors contribute ~~�20~~% to basal synaptic transmission		GluR2/3 receptors contribute 20% to basal synaptic transmission


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	Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from WT animals at the age of 2–4 weeks under basal conditions.		Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from WT animals at the age of 2–4 weeks under basal conditions.

	Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to �50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused an ~~�50~~% loss of AMPAR EPSCs.		Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to �50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused an 50% loss of AMPAR EPSCs.


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	ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE		ORGANOTYPIC HIPPOCAMPAL SLICE CULTURE

	Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to ~~�50~~% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2fl/fl mice also showed that loss of GluA2 caused an ~~�50~~% loss of AMPAR EPSCs.		Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to 50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2fl/fl mice also showed that loss of GluA2 caused an 50% loss of AMPAR EPSCs.

	Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.		Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.
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	Following the expression of Cre in GRIA1fl/fl hippocampal slice cultures, there was a gradual decrease in AMPAR EPSC amplitudes that stabilized at ~~�20~~% of control values at ~~�14~~ days after transfection. The scatter plot shows that there was an 80% loss of the AMPAR EPSCs.		Following the expression of Cre in GRIA1fl/fl hippocampal slice cultures, there was a gradual decrease in AMPAR EPSC amplitudes that stabilized at 20% of control values at 14 days after transfection. The scatter plot shows that there was an 80% loss of the AMPAR EPSCs.

	To analyze the mechanism for reduced AMPAR EPSCs, we recorded mEPSCs. There was a clear decrease in the amplitude of mEPSCs, as well as a decrease in frequency, indicating that there is a loss of AMPARs from all synapses.		To analyze the mechanism for reduced AMPAR EPSCs, we recorded mEPSCs. There was a clear decrease in the amplitude of mEPSCs, as well as a decrease in frequency, indicating that there is a loss of AMPARs from all synapses.

	These data suggest that GluR1/2 heteromers account for approximately 80% of synaptic AMPARs and GluR2/3 receptors contribute ~~�20~~% to basal synaptic transmission.		These data suggest that GluR1/2 heteromers account for approximately 80% of synaptic AMPARs and GluR2/3 receptors contribute 20% to basal synaptic transmission.

	Deletion of GluA1 resulted in a 95% loss of extrasynaptic receptors. The I/V of the remaining current was linear, indicating that the remaining receptors are primarily GluA2A3 heteromers. Compared to the profound loss of extrasynaptic current (~~�95~~%), synaptic currents were less impaired (80%) in GluA1-deleted cells, suggesting that synapses are capable of consolidating the few remaining GluA2A3 heteromers.		Deletion of GluA1 resulted in a 95% loss of extrasynaptic receptors. The I/V of the remaining current was linear, indicating that the remaining receptors are primarily GluA2A3 heteromers. Compared to the profound loss of extrasynaptic current (95%), synaptic currents were less impaired (80%) in GluA1-deleted cells, suggesting that synapses are capable of consolidating the few remaining GluA2A3 heteromers.



	~~[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|600px]]~~
	~~[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|600px]]~~
	~~[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|600px]]~~
	~~[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|600px]]~~
	~~[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|600px]]~~




			{{Clear}}
	{{Article\|Granger, Shi, Lu, Nicoll\|2011\|Nature - [http://www.nature.com/doifinder/10.1038/nature11775 FullText]\|23235828\|LTP requires a reserve pool of glutamate receptors independent of subunit type.}}		{{Article\|Granger, Shi, Lu, Nicoll\|2011\|Nature - [http://www.nature.com/doifinder/10.1038/nature11775 FullText]\|23235828\|LTP requires a reserve pool of glutamate receptors independent of subunit type.}}

Bradley Monk at 07:02, 21 March 2015

2015-03-21T07:02:33Z

@@ Line 6: / Line 6: @@
-We found that approximately 80% of synaptic and >95% of somatic extrasynaptic receptors are GluA1A2 heteromers. The remaining receptors are GluA2A3 heteromers.
+All WT AMPARs contain GluA2.
-Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from animals at the age of 2–4 weeks under basal conditions.
+GluR1/2 heteromers compose
-The profound loss of functional synaptic AMPARs following the ablation of GluA1, coupled with the fact that the I/V of the synaptic currents remains linear, suggests that GluA2A3 receptors contribute 20% to basal synaptic transmission.
+GluR2/3 receptors contribute �20% to basal synaptic transmission
 Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.
-[[File:Lu_Nicoll_2009_FIG2.jpg|800px]]
+[[File:Lu_Nicoll_2009_FIG2.jpg|thumb|600px]]

Bradley Monk at 02:50, 21 March 2015

2015-03-21T02:50:07Z

← Older revision		Revision as of 19:50, 20 March 2015
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	Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.		Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.


			[[File:Lu_Nicoll_2009_FIG2.jpg\|800px]]

Bradley Monk at 02:17, 21 March 2015

2015-03-21T02:17:51Z

← Older revision		Revision as of 19:17, 20 March 2015
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	==Journal Articles==		==Journal Articles==
			<br><br>

	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}

Bradley Monk at 02:17, 21 March 2015

2015-03-21T02:17:12Z

← Older revision		Revision as of 19:17, 20 March 2015
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	~~<big><big>[http://profiles.ucsf.edu/roger.nicoll Roger Nicoll UCSF Profile]</big></big>~~		==Journal Articles==

	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}

Bradley Monk at 02:08, 21 March 2015

2015-03-21T02:08:39Z

← Older revision		Revision as of 19:08, 20 March 2015
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	[[Category:Malinow]][[Category:Journals]] [[Category:Synaptic Plasticity]]		[[Category:Malinow]][[Category:Journals]] [[Category:Synaptic Plasticity]][[Category:Nicoll]]

Bradley Monk at 01:44, 21 March 2015

2015-03-21T01:44:38Z

← Older revision		Revision as of 18:44, 20 March 2015
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	<big><big>[http://profiles.ucsf.edu/roger.nicoll Roger Nicoll UCSF Profile]</big></big>		<big><big>[http://profiles.ucsf.edu/roger.nicoll Roger Nicoll UCSF Profile]</big></big>

	{{Article\|Lu, ~~Gray, Granger, During~~, Nicoll\|~~2011~~\|~~J Neurophysiol~~ - [http://www.~~ncbi~~.~~nlm.nih.gov~~/~~pubmed~~/~~20980546 PDF~~]\|~~20980546~~\|~~Potentiation~~ of synaptic AMPA receptors ~~induced~~ by ~~the deletion of NMDA receptors requires the GluA2 subunit~~}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}


			We found that approximately 80% of synaptic and >95% of somatic extrasynaptic receptors are GluA1A2 heteromers. The remaining receptors are GluA2A3 heteromers.

			Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from animals at the age of 2–4 weeks under basal conditions.

			The profound loss of functional synaptic AMPARs following the ablation of GluA1, coupled with the fact that the I/V of the synaptic currents remains linear, suggests that GluA2A3 receptors contribute 20% to basal synaptic transmission.

			Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to 50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused a 50% loss of AMPAR EPSCs.


			Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.




			{{Article\|Granger, Shi, Lu, Nicoll\|2011\|Nature - [http://www.nature.com/doifinder/10.1038/nature11775 FullText]\|23235828\|LTP requires a reserve pool of glutamate receptors independent of subunit type.}}

Bradley Monk at 01:27, 21 March 2015

2015-03-21T01:27:00Z

← Older revision		Revision as of 18:27, 20 March 2015
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	{{Article\|Lu, Gray, Granger, During, Nicoll\|2011\|J Neurophysiol - [http://www.ncbi.nlm.nih.gov/pubmed/20980546 PDF]\|20980546\|Potentiation of synaptic AMPA receptors induced by the deletion of NMDA receptors requires the GluA2 subunit}}		{{Article\|Lu, Gray, Granger, During, Nicoll\|2011\|J Neurophysiol - [http://www.ncbi.nlm.nih.gov/pubmed/20980546 PDF]\|20980546\|Potentiation of synaptic AMPA receptors induced by the deletion of NMDA receptors requires the GluA2 subunit}}
	~~{{ExpandBox\|expand to view study notes\|~~

	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\| [[File:Nicoll2011 Fig1.png]] }} 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\| [[File:Nicoll2011 Fig1.png]] }}. 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\| [[File:Nicoll2011 Fig1.png]] }}. Therefore in contrast to GluA1, the GluA2 subunit is critical for synaptic potentiation of AMPARs following NMDAR deletion.


	}}


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	<!-- ###################################### -->		<!-- ###################################### -->
	~~==Articles==~~
	~~<!-- * {{Pop3\|[[File:Dot.png]]\|<html><video src="XXXXXX" controls></video> <br> <div style='color:white; width:400px'> XXXXX </div></html>\|\|<big>SI video1 </big>}} -->~~


	{{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>~~

	~~{{Pop3\|[[File:Dot.png]]\|<html><video src="http://www.bradleymonk.com/w/images/1/18/Kasai_GluUncaging_S7.mov" controls></video> <br> <div style='color:white; width:400px'> Movie S7.~~
	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>}}





	{{Clear}}		{{Clear}}
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	</pre>		</pre>

			<pre>
	{{Ref\|Ehrlich Malinow\|14749436}}		{{Ref\|Ehrlich Malinow\|14749436}}
			{{Fig\| [[File:Nicoll2011 Fig1.png]] }}
			{{Pop3\|[[File:Dot.png]]\|<html><video src="XXXXXX" controls></video> <br> <div style='color:white; width:400px'> XXXXX </div></html>\|\|<big>SI video1 </big>}}
			<mediaplayer image='FULL_URL_PREVIEW_IMAGE' width='500' height='300'>FULL_URL_MOV</mediaplayer>
			</pre>

← Older revision		Revision as of 00:06, 21 March 2015
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	{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}		{{Article\|Lu, Shi, Nicoll\|2009\|Cell - [http://www.sciencedirect.com/science/article/pii/S0896627309002554 FullText]\|19409270\|Subunit composition of synaptic AMPA receptors revealed by a single-cell genetic approach}}

	[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG2.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG3.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG4.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG5.jpg\|thumb\|400px]]
	[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|~~500px~~]]		[[File:Lu_Nicoll_2009_FIG6.jpg\|thumb\|400px]]

	All WT AMPARs contain GluA2.		All WT AMPARs contain GluA2.