AMPA Receptor - Revision history

Bradley Monk at 01:44, 25 April 2015

2015-04-25T01:44:06Z

← Older revision		Revision as of 18:44, 24 April 2015
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	[[Category:Synaptic Plasticity]] [[Category:Journals]]		[[Category:Synaptic Plasticity]] [[Category:Journals]]
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	~~<br>~~ <br>		<br>

	{{~~Article\|Hayashi Malinow\|2000\|Science • [http~~:~~//www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]~~\|~~10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.~~}}		{{#section:Articles\|Hayashi_Malinow_2000_Science}}

	* Primary Model: Organotypic hippocampal slice culture. Sindbis virus expression system.		* Primary Model: Organotypic hippocampal slice culture. Sindbis virus expression system.
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	~~{{#section:Articles\|Hayashi_Malinow_2000_Science}}~~

Bradley Monk at 01:42, 25 April 2015

2015-04-25T01:42:36Z

← Older revision		Revision as of 18:42, 24 April 2015
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	{{:Articles#Hayashi_Malinow_2000_Science}}		{{#section:Articles\|Hayashi_Malinow_2000_Science}}

Bradley Monk: /* Surface & Synaptic Expression of GluR Subtypes */

2015-04-25T01:27:28Z

Surface & Synaptic Expression of GluR Subtypes

← Older revision		Revision as of 18:27, 24 April 2015
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	[[Category:Synaptic Plasticity]] [[Category:Journals]]		[[Category:Synaptic Plasticity]] [[Category:Journals]]
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			<br> <br>

	{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}		{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}
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	; Brads Notes		; Brads Notes on -- Hayashi, Malinow (2000) ''Science''

	It's interesting that Sindbis expression of GluR1-GFP in these organotypic hippocampal slice cultures had no effect on either the amplitude or rectification of (the putative ''basal-level'') synaptic transmission. This observation should not be overlooked when comparing the observations reported in this study with other studies examining whether GluR1 enters ''basal'' synapses.		It's interesting that Sindbis expression of GluR1-GFP in these organotypic hippocampal slice cultures had no effect on either the amplitude or rectification of (the putative ''basal-level'') synaptic transmission. This observation should not be overlooked when comparing the observations reported in this study with other studies examining whether GluR1 enters ''basal'' synapses.


			{{:Articles#Hayashi_Malinow_2000_Science}}

Bradley Monk: /* Surface & Synaptic Expression of GluR Subtypes */

2015-04-25T01:02:36Z

Surface & Synaptic Expression of GluR Subtypes

← Older revision		Revision as of 18:02, 24 April 2015
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	{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}		{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}

	* Organotypic hippocampal slice culture		* Primary Model: Organotypic hippocampal slice culture. Sindbis virus expression system.
	* Sindbis virus expression system		* Overexpression of GluR1-GFP had no effect on either the amplitude or rectification of (basal) synaptic transmission.
	* Overexpression of GluR1 had no effect on either the amplitude or rectification of (basal) synaptic transmission.		* When both GluR1 and tCaMKII we coexpressed, pairwise recordings from infected and noninfected cells showed that transmission was enhanced and had increased rectification
	* When both GluR1 and tCaMKII we coexpressed, pairwise recordings from infected and noninfected cells showed that transmission was enhanced and ~~showed~~ increased rectification~~, indicating a~~ contribution of homomeric GluR1 to transmission.		** indicates contribution of homomeric GluR1 to transmission.
			** rectification was due to coexpression of the two proteins since transmission onto cells expressing either tCaMKII or GluR1-GFP alone had rectification comparable to uninfected cells.
			* The last three amino acids of the GluR1 Ctail are TGL, which conforms to a PDZ ligand consensus sequence. They mutated the GluR1 Ctail from TGL to AGL creating GluR1(T887A).
			** This construct showed no effect on transmission when expressed alone.
			** When GluR1(T887A) was coexpressed with tCaMKII in hippocampal slice neurons, tCaMKII effects on synaptic response amplitude and rectification were completely blocked (transmission onto these neurons was actually depressed).


			; Brads Notes

			It's interesting that Sindbis expression of GluR1-GFP in these organotypic hippocampal slice cultures had no effect on either the amplitude or rectification of (the putative ''basal-level'') synaptic transmission. This observation should not be overlooked when comparing the observations reported in this study with other studies examining whether GluR1 enters ''basal'' synapses.

Bradley Monk: /* Surface & Synaptic Expression of GluR Subtypes */

2015-04-25T00:42:57Z

Surface & Synaptic Expression of GluR Subtypes

← Older revision		Revision as of 17:42, 24 April 2015
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	{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}		{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}

			* Organotypic hippocampal slice culture
			* Sindbis virus expression system
			* Overexpression of GluR1 had no effect on either the amplitude or rectification of (basal) synaptic transmission.
			* When both GluR1 and tCaMKII we coexpressed, pairwise recordings from infected and noninfected cells showed that transmission was enhanced and showed increased rectification, indicating a contribution of homomeric GluR1 to transmission.


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

Bradley Monk at 00:28, 25 April 2015

2015-04-25T00:28:26Z

← Older revision		Revision as of 17:28, 24 April 2015
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	==Surface & Synaptic Expression of GluR Subtypes==		==Surface & Synaptic Expression of GluR Subtypes==
	{{Article\|~~Testa Urban Hell~~\|~~2012~~\|~~Cell~~ • [http://www.~~sciencedirect~~.~~com/science~~/~~article~~/~~pii/S0896627312007192~~ PDF]\|~~22998868~~\|~~Nanoscopy of living brain slices with low light levels~~.}}		<!--
	;Figure 3		{{Article\|Hayashi, Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}
			;Figure 1
	RESOLFT Nanoscopy Reveals Actin Distribution within Dendritic Spines		RESOLFT Nanoscopy Reveals Actin Distribution within Dendritic Spines
	[[Category:Synaptic Plasticity]] [[Category:Journals]]		[[Category:Synaptic Plasticity]] [[Category:Journals]]
			-->

			{{Article\|Hayashi Malinow\|2000\|Science • [http://www.ncbi.nlm.nih.gov/pubmed/10731148 PDF]\|10731148\|Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction.}}

Bradley Monk at 00:25, 25 April 2015

2015-04-25T00:25:21Z

← Older revision		Revision as of 17:25, 24 April 2015
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	;Quick Facts

			==Surface & Synaptic Expression of GluR Subtypes==
			{{Article\|Testa Urban Hell\|2012\|Cell • [http://www.sciencedirect.com/science/article/pii/S0896627312007192 PDF]\|22998868\|Nanoscopy of living brain slices with low light levels.}}
			;Figure 3
			RESOLFT Nanoscopy Reveals Actin Distribution within Dendritic Spines
			[[Category:Synaptic Plasticity]] [[Category:Journals]]




			<!-- ###################################### -->
			==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>}} -->






			==Quick Facts==

	*Most AMPARs in adult [[hippocampus]] and cortex appear to consist of the GluA1 plus GluA2, or GluA2 plus GluA3 subunits. Since GluA3 is expressed at relatively low levels, '''over 70% of GluA2 is associated with GluA1'''		*Most AMPARs in adult [[hippocampus]] and cortex appear to consist of the GluA1 plus GluA2, or GluA2 plus GluA3 subunits. Since GluA3 is expressed at relatively low levels, '''over 70% of GluA2 is associated with GluA1'''

Bradley Monk: /* Experimental Goals */

2014-08-10T00:59:01Z

Experimental Goals

← Older revision		Revision as of 17:59, 9 August 2014
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	ZIP is a designer molecule that has been shown to inactivate [[PKMz]]. There are several high-profile reports of successfully using ZIP to abolish a learned behavior. These experiments have failed replication on several accounts. If ZIP inactivates [[PKMz]], this should be reflected by a relatively long-lasting decrease in [[AMPAR]] density. This is what I am interested in exploring. I want to know how to effectively use ZIP as a tool to understand memory maintenance and network properties of memory engrams.		ZIP is a designer molecule that has been shown to inactivate [[PKMz]]. There are several high-profile reports of successfully using ZIP to abolish a learned behavior. These experiments have failed replication on several accounts. If ZIP inactivates [[PKMz]], this should be reflected by a relatively long-lasting decrease in [[AMPAR]] density. This is what I am interested in exploring. I want to know how to effectively use ZIP as a tool to understand memory maintenance and network properties of memory engrams.

	[[Category:Qual]]		[[Category:Qual]][[Category:Neurobiology]]

Bradley Monk at 02:32, 7 July 2013

2013-07-07T02:32:46Z

← Older revision		Revision as of 19:32, 6 July 2013
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	*That Q/R editing is essential for correct [[brain]] function and is demonstrated by the finding that '''mice engineered to synthesize only unedited GluA2''' subunits '''die''' early and '''develop seizures''', the same goes for '''ADAR2 knockout (KO) mice''' who '''also have seizures'''		*That Q/R editing is essential for correct [[brain]] function and is demonstrated by the finding that '''mice engineered to synthesize only unedited GluA2''' subunits '''die''' early and '''develop seizures''', the same goes for '''ADAR2 knockout (KO) mice''' who '''also have seizures'''


			<big>[[LTP]] Dynamics</big>

			;AMPARs:
			*GluA2 blocks calcium
			*GluA1 permits calcium
			*GluA2 trumps GluA1 (GluA2 is dominant phenotype)

			;Glutamate causes:
			*increased [[AMPAR]] synaptic diffusion rates
			*rapid [[AMPAR]] endocytosis

			;Calcium causes:
			*decreased [[AMPAR]] diffusion rates
			*increased [[AMPAR]] synaptic expression
			*blocking calcium increases [[AMPAR]] diffusion

			*Since GluA2 blocks calcium, it's presence in a synapse may destabilize the local potentiation status.

			;AMPARs vs. NMDAR diffusion
			*extrasynaptic: [[AMPAR]] 4x faster than NMDARs
			**(10.0 vs 2.3 nm/s)
			*synaptic: similar speeds
			**(28.0 vs 21.0 nm/s)
			*Note that diffusion was faster outside the synapse than inside the synapse (that doesn't make sense)

			;Neural Stimulation with KCl causes:
			*extrasynaptic AMPARs to diffuse 5x faster than baseline
			*synaptic [[AMPAR]] mobility didn't change

			;PKC activity (stimulated by TPA) causes:
			*extrasynaptic: [[AMPAR]] and NMDAR have significantly increased mobility
			*synaptic: [[AMPAR]] and NMDAR have significantly increased mobility

Bradley Monk at 02:16, 7 July 2013

2013-07-07T02:16:16Z

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