- 32-0400 - Invitrogen Antibodies GRIA3 antibody

Submitted references Hippocampal AMPA receptor assemblies and mechanism of allosteric inhibition.

Yu J, Rao P, Clark S, Mitra J, Ha T, Gouaux E
Nature 2021 Jun;594(7863):448-453

Cognitive aging is associated with redistribution of synaptic weights in the hippocampus.

Buss EW, Corbett NJ, Roberts JG, Ybarra N, Musial TF, Simkin D, Molina-Campos E, Oh KJ, Nielsen LL, Ayala GD, Mullen SA, Farooqi AK, D'Souza GX, Hill CL, Bean LA, Rogalsky AE, Russo ML, Curlik DM, Antion MD, Weiss C, Chetkovich DM, Oh MM, Disterhoft JF, Nicholson DA
Proceedings of the National Academy of Sciences of the United States of America 2021 Feb 23;118(8)

L-Stepholidine rescues memory deficit and synaptic plasticity in models of Alzheimer's disease via activating dopamine D1 receptor/PKA signaling pathway.

Hao JR, Sun N, Lei L, Li XY, Yao B, Sun K, Hu R, Zhang X, Shi XD, Gao C
Cell death & disease 2015 Nov 5;6(11):e1965

Differential trafficking of AMPA and NMDA receptors during long-term potentiation in awake adult animals.

Williams JM, Guévremont D, Mason-Parker SE, Luxmanan C, Tate WP, Abraham WC
The Journal of neuroscience : the official journal of the Society for Neuroscience 2007 Dec 19;27(51):14171-8

Involvement of the AMPA receptor GluR-C subunit in alcohol-seeking behavior and relapse.

Sanchis-Segura C, Borchardt T, Vengeliene V, Zghoul T, Bachteler D, Gass P, Sprengel R, Spanagel R
The Journal of neuroscience : the official journal of the Society for Neuroscience 2006 Jan 25;26(4):1231-8

Glutamate receptor subunit 3 (GluR3) immunoreactivity delineates a subpopulation of parvalbumin-containing interneurons in the rat hippocampus.

Moga DE, Janssen WG, Vissavajjhala P, Czelusniak SM, Moran TM, Hof PR, Morrison JH
The Journal of comparative neurology 2003 Jul 14;462(1):15-28

A juvenile form of postsynaptic hippocampal long-term potentiation in mice deficient for the AMPA receptor subunit GluR-A.

Jensen V, Kaiser KM, Borchardt T, Adelmann G, Rozov A, Burnashev N, Brix C, Frotscher M, Andersen P, Hvalby Ø, Sakmann B, Seeburg PH, Sprengel R
The Journal of physiology 2003 Dec 15;553(Pt 3):843-56

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 2 L-SPD rescues the decreased phosphorylation and surface expression of GluA1-containing AMPA receptors in the hippocampus of APP/PS1 mice. ( a ) Surface expression of GluA1 and GluA2 subunits were decreased, whereas S-GluA3 expression was not changed in APP/PS1 mice treated with vehicle. L-SPD significantly improved the levels of surface expression of GluA1 and GluA2 in APP/PS1 mice. (GluA1: n =4 in each group, GluA2: n =5 in each group, GluA3: n =4 in each group). ( b ) Total expression of GluA1, GluA2 and GluA3 subunits were not changed ( n =4 in each group). ( c ) Phosphorylated levels of both pS845 and pS831 of GluA1 were decreased in APP/PS1 mice treated with vehicle. L-SPD could improve the levels of both pS845 and pS831 ( n =4 in each group). ( d ) Phosphorylated levels of pS880 of GluA2 was not changed and L-SPD had no effect on pS880 in APP/PS1 mice ( n =3 in each group). ( e ) Phosphorylated levels of CaMKIIalpha was increased in APP /PS1 mice treated with vehicle. L-SPD had no effect on p-CaMKIIalpha ( n =6 in each group). * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4 Activation of D1/PKA rescues the decreased GluA1-containing AMPA receptor surface expression induced by ADDLs in cultured hippocampal neurons. ( a - c ) Surface expression of GluA1 (S-GluA1) and GluA2 (S-GluA2) were significantly decreased after treating with ADDLs (500 nM) for 3-24 h, whereas surface expression of GluA3 (S-GluA3) was not changed. Total expression of GluA1-3 (T-GluA) were not changed. (GluA1: n =5 in each group, GluA2: n =4 in each group, GluA3: n =4 in each group). ( d ) Phosphorylated levels of GluA1 at Serine 845 (pS845) and Serine 831 (pS831) were decreased after treating with ADDLs (pS845: n =9 in each group, pS831: n =9 in each group). ( e ) Pretreatment with PKA activator Sp-cAMPS (10 muM) rescued the decreased pS845 and surface expression of GluA1 induced by ADDLs, whereas the PKA inhibitor Rp-cAMPS (10 muM) reversed these effects. Sp-cAMPS or Rp-cAMPS was added 10 min before ADDLs ( n =4 in each group). ( f ) Pretreatment with D1-type receptor agonist SKF 81297 (SKF, 3 muM) rescued the decreased pS845 and surface expression of GluA1 induced by ADDLs, whereas the antagonist SCH 23390 (SCH, 10 muM) reversed these effects. SKF 81297 or SCH 23390 was added 15 min before ADDLs ( n =6 in each group). * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4. A , B , Changes in AMPA receptor subunit expression of the AMPA receptor subunits GluR-A, GluR-B, GluR-C, and GluR-D in hippocampus ( A ) and cerebellum ( B ) of wild-type (WT) and GluR-C knock-out (GluR-C -/-) mice from P2 to P90. Total proteins of the hippocampus and the cerebellum were isolated, and for each sample, 10 mug of protein was separated on a 7.5% SDS-PAGE and transferred on nitrocellulose. The glutamate receptor subunits were visualized by selective antibodies and monitored by autoradiography. The alpha-subunit of the Ca 2+ /calmodulin-dependent protein kinase II (alpha-CaMKII) and betaIII-tubulin (betaIII-Tub.) was used as a positive control for developmental controlled gene expression in hippocampus and cerebellum, respectively. Loading was controlled by beta-actin. The experiment was repeated with at least three sets of mice. One representative example for each subunit is given.

32-0400

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