The AMPA receptor-associated protein Shisa7 regulates hippocampal synaptic function and contextual memory

Schmitz, Leanne J M; Klaassen, Remco V.; Ruiperez-Alonso, Marta; Zamri, Azra Elia; Stroeder, Jasper; Rao-Ruiz, Priyanka; Lodder, J.C.; Loo, Rolinka J. van der; Mansvelder, Huibert D.; Smit, August B.; Spijker, Sabine

doi:10.7554/elife.24192

Cited by 40 publications

(54 citation statements)

References 69 publications

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“…GluR1 and GluR2 are major subunits of important excitable glutamate amino-acid-3-hydroxy-5-methyl-isoxazol-4-propionic acid receptors (AMPARs), which regulate synaptic plasticity and memory [71, 72]. GluR1 and GluR2 levels were not altered in our study.…”

Section: Discussionmentioning

confidence: 54%

Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

Yao

Zhang

et al. 2019

Neural Plasticity

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Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.

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Section: Discussionmentioning

confidence: 54%

Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

Yao

Zhang

et al. 2019

Neural Plasticity

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“…5 ). Of note, while not part of the native complexes as described by Schwenk and colleagues [ 10 ], Shisa7 has also recently been found to associate with AMPARs and regulate their synaptic function; Shisa7 knockout mice impaired LTP initiation and maintenance, and decreased short-term and long-term contextual fear memory [ 350 ]. As the expression pattern of Shisa6–9 is developmentally regulated and as they differentially regulate AMPAR trafficking and gating in a cell-type-dependent manner [ 344 ], additional studies are necessary to determine more precisely their specific role in the various different brain regions.…”

Section: Shisa6 and 9 (Cystine-knot Ampar Modulating Proteins (Ckamp)mentioning

confidence: 99%

AMPA receptors and their minions: auxiliary proteins in AMPA receptor trafficking

Bissen

Foss

Acker‐Palmer

2019

Cell. Mol. Life Sci.

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To correctly transfer information, neuronal networks need to continuously adjust their synaptic strength to extrinsic stimuli. This ability, termed synaptic plasticity, is at the heart of their function and is, thus, tightly regulated. In glutamatergic neurons, synaptic strength is controlled by the number and function of AMPA receptors at the postsynapse, which mediate most of the fast excitatory transmission in the central nervous system. Their trafficking to, at, and from the synapse, is, therefore, a key mechanism underlying synaptic plasticity. Intensive research over the last 20 years has revealed the increasing importance of interacting proteins, which accompany AMPA receptors throughout their lifetime and help to refine the temporal and spatial modulation of their trafficking and function. In this review, we discuss the current knowledge about the roles of key partners in regulating AMPA receptor trafficking and focus especially on the movement between the intracellular, extrasynaptic, and synaptic pools. We examine their involvement not only in basal synaptic function, but also in Hebbian and homeostatic plasticity. Included in our review are well-established AMPA receptor interactants such as GRIP1 and PICK1, the classical auxiliary subunits TARP and CNIH, and the newest additions to AMPA receptor native complexes.

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“…Some of these have been shown to fulfill the criteria of an auxiliary subunit. In particular, transmembrane AMPAR regulatory proteins (TARPs) ( Chen et al., 2000 , Tomita et al., 2004 ), cornichons ( Schwenk et al., 2009 ), Shisa6 ( Klaassen et al., 2016 ), Shisa7 ( Schmitz et al., 2017 ), and Shisa9 (CKAMP44) ( von Engelhardt et al., 2010 ) were shown to modify AMPAR biophysical properties, affect receptor trafficking, and/or trap receptors at the postsynaptic density (PSD).…”

Section: Introductionmentioning

confidence: 99%

Noelin1 Affects Lateral Mobility of Synaptic AMPA Receptors

et al. 2018

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SummaryLateral diffusion on the neuronal plasma membrane of the AMPA-type glutamate receptor (AMPAR) serves an important role in synaptic plasticity. We investigated the role of the secreted glycoprotein Noelin1 (Olfactomedin-1 or Pancortin) in AMPAR lateral mobility and its dependence on the extracellular matrix (ECM). We found that Noelin1 interacts with the AMPAR with high affinity, however, without affecting rise- and decay time and desensitization properties. Noelin1 co-localizes with synaptic and extra-synaptic AMPARs and is expressed at synapses in an activity-dependent manner. Single-particle tracking shows that Noelin1 reduces lateral mobility of both synaptic and extra-synaptic GluA1-containing receptors and affects short-term plasticity. While the ECM does not constrain the synaptic pool of AMPARs and acts only extrasynaptically, Noelin1 contributes to synaptic potentiation by limiting AMPAR mobility at synaptic sites. This is the first evidence for the role of a secreted AMPAR-interacting protein on mobility of GluA1-containing receptors and synaptic plasticity.

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The AMPA receptor-associated protein Shisa7 regulates hippocampal synaptic function and contextual memory

Cited by 40 publications

References 69 publications

Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

AMPA receptors and their minions: auxiliary proteins in AMPA receptor trafficking

Noelin1 Affects Lateral Mobility of Synaptic AMPA Receptors

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