1,270 results match your criteria protein ampars


Flavonoid fisetin reverses impaired hippocampal synaptic plasticity and cognitive function by regulating the function of AMPARs in a male rat model of schizophrenia.

J Neurochem 2021 Apr 21. Epub 2021 Apr 21.

Medical Experimental Center, Jiangxi Mental Hospital/Affiliated Mental Hospital of Nanchang University, Nanchang, 330029, P.R. China.

Cognitive deficits are the core feature of schizophrenia and effective treatment strategies are still missing. Previous studies have reported that fisetin promotes long-term potentiation (LTP) and cognitive function in normal rodents and other model animals of neurological diseases. The aim of the present study was to assess the effect of fisetin on synaptic plasticity and cognitive deficits caused by a brief disruption of N-methyl-D-aspartate receptors (NMDARs) with dizocilpine (MK-801) during early development in rats. Read More

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Secreted Amyloid Precursor Protein-Alpha Enhances LTP Through the Synthesis and Trafficking of Ca-Permeable AMPA Receptors.

Front Mol Neurosci 2021 1;14:660208. Epub 2021 Apr 1.

Department of Anatomy, Brain Health Research Centre, Brain Research New Zealand - Rangahau Roro Aotearoa, University of Otago, Dunedin, New Zealand.

Regulation of AMPA receptor expression by neuronal activity and neuromodulators is critical to the expression of both long-term potentiation (LTP) and memory. In particular, Ca-permeable AMPARs (CP-AMPAR) play a unique role in these processes due to their transient, activity-regulated expression at synapses. Secreted amyloid precursor protein-alpha (sAPPα), a metabolite of the parent amyloid precursor protein (APP) has been previously shown to enhance hippocampal LTP as well as memory formation in both normal animals and in Alzheimer's disease models. Read More

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EphrinB2 and GRIP1 stabilize mushroom spines during denervation-induced homeostatic plasticity.

Cell Rep 2021 Mar;34(13):108923

Institute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany; Max Planck Institute for Brain Research, Max von Laue Str. 4, 60438 Frankfurt am Main, Germany; Cardio-Pulmonary Institute (CPI), Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany. Electronic address:

Despite decades of work, much remains elusive about molecular events at the interplay between physiological and structural changes underlying neuronal plasticity. Here, we combined repetitive live imaging and expansion microscopy in organotypic brain slice cultures to quantitatively characterize the dynamic changes of the intracellular versus surface pools of GluA2-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) across the different dendritic spine types and the shaft during hippocampal homeostatic plasticity. Mechanistically, we identify ephrinB2 and glutamate receptor interacting protein (GRIP) 1 as mediating AMPAR relocation to the mushroom spine surface following lesion-induced denervation. Read More

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A Role for Transmembrane Protein 16C/Slack Impairment in Excitatory Nociceptive Synaptic Plasticity in the Pathogenesis of Remifentanil-induced Hyperalgesia in Rats.

Neurosci Bull 2021 Mar 29. Epub 2021 Mar 29.

Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Research Institute of Anesthesiology, Tianjin, 300052, China.

Remifentanil is widely used to control intraoperative pain. However, its analgesic effect is limited by the generation of postoperative hyperalgesia. In this study, we investigated whether the impairment of transmembrane protein 16C (TMEM16C)/Slack is required for α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) activation in remifentanil-induced postoperative hyperalgesia. Read More

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Targeting redox-altered plasticity to reactivate synaptic function: A novel therapeutic strategy for cognitive disorder.

Acta Pharm Sin B 2021 Mar 24;11(3):599-608. Epub 2020 Nov 24.

Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Redox-altered plasticity refers to redox-dependent reversible changes in synaptic plasticity altering functions of key proteins, such as -methyl-d-aspartate receptor (NMDAR). Age-related cognitive disorders includes Alzheimer's disease (AD), vascular dementia (VD), and age-associated memory impairment (AAMI). Based on the critical role of NMDAR-dependent long-term potentiation (LTP) in memory, the increase of reactive oxygen species in cognitive disorders, and the sensitivity of NMDAR to the redox status, converging lines have suggested the redox-altered NMDAR-dependent plasticity might underlie the synaptic dysfunctions associated with cognitive disorders. Read More

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Membrane Remodeling by Arc/Arg3.1.

Front Mol Biosci 2021 8;8:630625. Epub 2021 Mar 8.

Department of Cell and Molecular Biology, University of Hawaii at Manoa, Honolulu, HI, United States.

The activity-regulated cytoskeletal-associated protein (Arc, also known as Arg3.1) is an immediate early gene product induced by activity/experience and required for multiple modes of synaptic plasticity. Both long-term potentiation (LTP) and long-term depression (LTD) are impaired upon Arc deletion, as well as the ability to form long-term spatial, taste and fear memories. Read More

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Decreased neuronal synaptosome associated protein 29 contributes to poststroke cognitive impairment by disrupting presynaptic maintenance.

Theranostics 2021 4;11(10):4616-4636. Epub 2021 Mar 4.

Department of Neurobiology, Department of Physiology and Pathophysiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.

Poststroke cognitive impairments are common in stroke survivors, and pose a high risk of incident dementia. However, the cause of these cognitive impairments is obscure and required an investigation. Oxygen-glucose deprivation (OGD) model and middle cerebral artery occlusion (MCAO) model were used to imitate or acute cerebral ischemia, respectively. Read More

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An optimized CRISPR/Cas9 approach for precise genome editing in neurons.

Elife 2021 Mar 10;10. Epub 2021 Mar 10.

Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States.

The efficient knock-in of large DNA fragments to label endogenous proteins remains especially challenging in non-dividing cells such as neurons. We developed argeted nock-n with wo (TKIT) guides as a novel CRISPR/Cas9 based approach for efficient, and precise, genomic knock-in. Through targeting non-coding regions TKIT is resistant to INDEL mutations. Read More

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The WD40-Repeat Protein WDR-20 and the Deubiquitinating Enzyme USP-46 Promote Cell Surface Levels of Glutamate Receptors.

J Neurosci 2021 Apr 23;41(14):3082-3093. Epub 2021 Feb 23.

Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, Massachusetts 02111

Reversible modification of AMPA receptors (AMPARs) with ubiquitin regulates receptor levels at synapses and controls synaptic strength. The conserved deubiquitinating enzyme (DUB) ubiquitin-specific protease-46 (USP-46) removes ubiquitin from AMPARs and protects them from degradation in both and mammals. Although DUBs are critical for diverse physiological processes, the mechanisms that regulate DUBs, especially in the nervous system, are not well understood. Read More

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Ligand-directed two-step labeling to quantify neuronal glutamate receptor trafficking.

Nat Commun 2021 02 5;12(1):831. Epub 2021 Feb 5.

Department of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, 464-8603, Japan.

The regulation of glutamate receptor localization is critical for development and synaptic plasticity in the central nervous system. Conventional biochemical and molecular biological approaches have been widely used to analyze glutamate receptor trafficking, especially for α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate-type glutamate receptors (AMPARs). However, conflicting findings have been reported because of a lack of useful tools for analyzing endogenous AMPARs. Read More

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February 2021

Stress undermines reward-guided cognitive performance through synaptic depression in the lateral habenula.

Neuron 2021 03 2;109(6):947-956.e5. Epub 2021 Feb 2.

The Department of Fundamental Neuroscience, The University of Lausanne, 1005 Lausanne, Switzerland; Inserm, UMR-S 839, 75005 Paris, France. Electronic address:

Weighing alternatives during reward pursuit is a vital cognitive computation that, when disrupted by stress, yields aspects of neuropsychiatric disorders. To examine the neural mechanisms underlying these phenomena, we employed a behavioral task in which mice were confronted by a reward and its omission (i.e. Read More

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Amygdala-hippocampal innervation modulates stress-induced depressive-like behaviors through AMPA receptors.

Proc Natl Acad Sci U S A 2021 Feb;118(6)

Neuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory for Neuroscience, Ministry of Education/National Health Commission of People's Republic of China, IDG/McGovern Institute for Brain Research at Peking University, 100083 Beijing, People's Republic of China;

Chronic stress is one of the most critical factors in the onset of depressive disorders; hence, environmental factors such as psychosocial stress are commonly used to induce depressive-​like traits in animal models of depression. Ventral CA1 (vCA1) in hippocampus and basal lateral amygdala (BLA) are critical sites during chronic stress-induced alterations in depressive subjects; however, the underlying neural mechanisms remain unclear. Here we employed chronic unpredictable mild stress (CUMS) to model depression in mice and found that the activity of the posterior BLA to vCA1 (pBLA-vCA1) innervation was markedly reduced. Read More

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February 2021

Cocaine-seeking behaviour is differentially expressed in male and female mice exposed to maternal separation and is associated with alterations in AMPA receptors subunits in the medial prefrontal cortex.

Prog Neuropsychopharmacol Biol Psychiatry 2021 Jan 23;109:110262. Epub 2021 Jan 23.

Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain; Neuroscience Research Program, IMIM-Hospital del Mar Research Institute, Barcelona, Spain. Electronic address:

According with clinical data, women evolve differently from drug use to drug abuse. Among drugs of abuse, cocaine is the most consumed psychostimulant. Animal studies demonstrated that females show increased motivation to seek cocaine during the self-administration paradigm (SA) than males. Read More

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January 2021

Oxidative Stress Underlies the Ischemia/Reperfusion-Induced Internalization and Degradation of AMPA Receptors.

Int J Mol Sci 2021 Jan 13;22(2). Epub 2021 Jan 13.

Department of Pharmaceutical Sciences and Molecular Medicine, Washington State University-Health Sciences, Spokane, WA 99201, USA.

Stroke is the fifth leading cause of death annually in the United States. Ischemic stroke occurs when a blood vessel supplying the brain is occluded. The hippocampus is particularly susceptible to AMPA receptor-mediated delayed neuronal death as a result of ischemic/reperfusion injury. Read More

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January 2021

Adenosine Signaling and Clathrin-Mediated Endocytosis of Glutamate AMPA Receptors in Delayed Hypoxic Injury in Rat Hippocampus: Role of Casein Kinase 2.

Mol Neurobiol 2021 May 7;58(5):1932-1951. Epub 2021 Jan 7.

Department of Surgery, Neuroscience Research Cluster, College of Medicine, University of Saskatchewan, Room GD30.4, D-Wing Health Science Building, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.

Chronic adenosine A1R stimulation in hypoxia leads to persistent hippocampal synaptic depression, while unopposed adenosine A2AR receptor stimulation during hypoxia/reperfusion triggers adenosine-induced post-hypoxia synaptic potentiation (APSP) and increased neuronal death. Still, the mechanisms responsible for this adenosine-mediated neuronal damage following hypoxia need to be fully elucidated. We tested the hypothesis that A1R and A2AR regulation by protein kinase casein kinase 2 (CK2) and clathrin-dependent endocytosis of AMPARs both contribute to APSPs and neuronal damage. Read More

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Clmp Regulates AMPA and Kainate Receptor Responses in the Neonatal Hippocampal CA3 and Kainate Seizure Susceptibility in Mice.

Front Synaptic Neurosci 2020 21;12:567075. Epub 2020 Dec 21.

Center for Synaptic Brain Dysfunctions, Institute for Basic Science, Daejeon, South Korea.

Synaptic adhesion molecules regulate synapse development through trans-synaptic adhesion and assembly of diverse synaptic proteins. Many synaptic adhesion molecules positively regulate synapse development; some, however, exert negative regulation, although such cases are relatively rare. In addition, synaptic adhesion molecules regulate the amplitude of post-synaptic receptor responses, but whether adhesion molecules can regulate the kinetic properties of post-synaptic receptors remains unclear. Read More

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December 2020

Transient Enhanced GluA2 Expression in Young Hippocampal Neurons of a Fragile X Mouse Model.

Front Synaptic Neurosci 2020 3;12:588295. Epub 2020 Dec 3.

Department of Physiology and Biophysics, University of Washington, Seattle, WA, United States.

AMPA-type glutamate receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits and play important roles in synaptic transmission and plasticity. Here, we have investigated the development of AMPAR-mediated synaptic transmission in the hippocampus of the Fmr1 knock-out (KO) mouse, a widely used model of Fragile X syndrome (FXS). FXS is the leading monogenic cause of intellectual disability and autism spectrum disorders (ASD) and it is considered a neurodevelopmental disorder. Read More

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December 2020

Effect of Aggressive Experience in Female Syrian Hamsters on Glutamate Receptor Expression in the Nucleus Accumbens.

Front Behav Neurosci 2020 23;14:583395. Epub 2020 Nov 23.

Department of Neuroscience, University of Minnesota, Minneapolis, MN, United States.

Our social relationships determine our health and well-being. In rodent models, there is now strong support for the rewarding properties of aggressive or assertive behaviors to be critical for the expression and development of adaptive social relationships, buffering from stress and protecting from the development of psychiatric disorders such as depression. However, due to the false belief that aggression is not a part of the normal repertoire of social behaviors displayed by females, almost nothing is known about the neural mechanisms mediating the rewarding properties of aggression in half the population. Read More

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November 2020

The Requirement of the C-Terminal Domain of GluA1 in Different Forms of Long-Term Potentiation in the Hippocampus Is Age-Dependent.

Front Synaptic Neurosci 2020 30;12:588785. Epub 2020 Oct 30.

Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.

Long-term potentiation (LTP) at glutamatergic synapses is an extensively studied form of long-lasting synaptic plasticity widely regarded as the cellular basis for learning and memory. At the CA1 synapse, there are multiple forms of LTP with distinct properties. Although AMPA glutamate receptors (AMPARs) are a key target of LTP expression, whether they are required in all forms of LTP remains unclear. Read More

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October 2020

AMPA Receptor Surface Expression Is Regulated by S-Nitrosylation of Thorase and Transnitrosylation of NSF.

Cell Rep 2020 11;33(5):108329

Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, University of Massachusetts School of Medicine, Worcester, MA 01655, USA; Graduate Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address:

The regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) trafficking affects multiple brain functions, such as learning and memory. We have previously shown that Thorase plays an important role in the internalization of AMPARs from the synaptic membrane. Here, we show that N-methyl-d-aspartate receptor (NMDAR) activation leads to increased S-nitrosylation of Thorase and N-ethylmaleimide-sensitive factor (NSF). Read More

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November 2020

Age-Dependent Shift of AMPA Receptors From Synapses to Intracellular Compartments in Alzheimer's Disease: Immunocytochemical Analysis of the CA1 Hippocampal Region in APP/PS1 Transgenic Mouse Model.

Front Aging Neurosci 2020 6;12:577996. Epub 2020 Oct 6.

Synaptic Structure Laboratory, Departamento de Ciencias Médicas, Facultad de Medicina, Instituto de Investigación en Discapacidades Neurológicas (IDINE), Universidad de Castilla-La Mancha, Albacete, Spain.

Synapse loss occurs early in Alzheimer's disease (AD) patients and animal models. Alterations at synaptic level are a major morphological correlate of the memory deficits and related symptoms of AD. Given the predominant roles of synaptic AMPA receptors (AMPARs) in excitatory synaptic transmission in the brain, changes in their dynamic regulation are also implicated in the pathophysiology of AD. Read More

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October 2020

Co-treatment of AMPA endocytosis inhibitor and GluN2B antagonist facilitate consolidation and retrieval of memory impaired by β amyloid peptide.

Int J Neurosci 2020 Oct 28:1-10. Epub 2020 Oct 28.

Cellular & Molecular Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.

Background: Glutamate neurotransmission stands as an important issue to minimize memory impairment. We investigated the effects of an inhibitor of α-amino-3-hydroxy-5-methyl-4-isozazole propionic acid receptors (AMPA) endocytosis and GluN2B subunit of N-methyl-d-aspartate receptors (NMDA), either isolated or combined, on memory impairments induced by Amyloid beta1-42 (Aβ).

Methods: Eighty male Wistar rats were used for two experiments of consolidation and retrieval of memory. Read More

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October 2020

AMPA receptor auxiliary subunits emerged during early vertebrate evolution by neo/subfunctionalization of unrelated proteins.

Open Biol 2020 10 28;10(10):200234. Epub 2020 Oct 28.

Molecular Physiology of the Synapse Laboratory, Biomedical Research Institute Sant Pau, Barcelona, Spain.

In mammalian synapses, the function of ionotropic glutamate receptors is critically modulated by auxiliary subunits. Most of these specifically regulate the synaptic localization and electrophysiological properties of AMPA-type glutamate receptors (AMPARs). Here, we comprehensively investigated the animal evolution of the protein families that contain AMPAR auxiliary subunits (ARASs). Read More

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October 2020

Ethanol neurotoxicity is mediated by changes in expression, surface localization and functional properties of glutamate AMPA receptors.

J Neurochem 2020 Oct 26. Epub 2020 Oct 26.

Department of Neuroscience, Psychology, Drug Research and Child Health (NeuroFarBa), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.

Modifications in the subunit composition of AMPA receptors (AMPARs) have been linked to the transition from physiological to pathological conditions in a number of contexts, including EtOH-induced neurotoxicity. Previous work from our laboratory showed that EtOH withdrawal causes CA1 pyramidal cell death in organotypic hippocampal slices and changes in the expression of AMPARs. Here, we investigated whether changes in expression and function of AMPARs may be causal for EtOH-induced neurotoxicity. Read More

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October 2020

Activity Dependent Inhibition of AMPA Receptors by Zn.

J Neurosci 2020 11 12;40(45):8629-8636. Epub 2020 Oct 12.

Center for Membrane Biology, Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston, Houston, Texas 77030

Zn has been shown to have a wide range of modulatory effects on neuronal AMPARs. However, the mechanism of modulation is largely unknown. Here we show that Zn inhibits GluA2(Q) homomeric receptors in an activity- and voltage-dependent manner, indicating a pore block mechanism. Read More

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November 2020

PORCN Negatively Regulates AMPAR Function Independently of Subunit Composition and the Amino-Terminal and Carboxy-Terminal Domains of AMPARs.

Front Cell Dev Biol 2020 25;8:829. Epub 2020 Aug 25.

PKU-IDG/McGovern Institute for Brain Research, School of Life Sciences, Peking University, Beijing, China.

Most fast excitatory synaptic transmissions in the mammalian brain are mediated by α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (AMPARs), which are ligand-gated cation channels. The membrane expression level of AMPARs is largely determined by auxiliary subunits in AMPAR macromolecules, including porcupine O-acyltransferase (PORCN), which negatively regulates AMPAR trafficking to the plasma membrane. However, whether PORCN-mediated regulation depends on AMPAR subunit composition or particular regions of a subunit has not been determined. Read More

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GRIP1 regulates synaptic plasticity and learning and memory.

Proc Natl Acad Sci U S A 2020 10 18;117(40):25085-25091. Epub 2020 Sep 18.

Solomon H. Snyder Department of Neuroscience and Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205;

Hebbian plasticity is a key mechanism for higher brain functions, such as learning and memory. This form of synaptic plasticity primarily involves the regulation of synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) abundance and properties, whereby AMPARs are inserted into synapses during long-term potentiation (LTP) or removed during long-term depression (LTD). The molecular mechanisms underlying AMPAR trafficking remain elusive, however. Read More

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October 2020

Sensing of nutrients by CPT1C controls SAC1 activity to regulate AMPA receptor trafficking.

J Cell Biol 2020 10;219(10)

Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya, Sant Cugat del Vallès, Spain.

Carnitine palmitoyltransferase 1C (CPT1C) is a sensor of malonyl-CoA and is located in the ER of neurons. AMPA receptors (AMPARs) mediate fast excitatory neurotransmission in the brain and play a key role in synaptic plasticity. In the present study, we demonstrate across different metabolic stress conditions that modulate malonyl-CoA levels in cortical neurons that CPT1C regulates the trafficking of the major AMPAR subunit, GluA1, through the phosphatidyl-inositol-4-phosphate (PI(4)P) phosphatase SAC1. Read More

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October 2020

Mechanism underlying hippocampal long-term potentiation and depression based on competition between endocytosis and exocytosis of AMPA receptors.

Sci Rep 2020 09 7;10(1):14711. Epub 2020 Sep 7.

Department of Computer Science and Engineering, Toyohashi University of Technology, 1-1 Hibarigaoka, Tempaku-cho, Toyohashi, Aichi, 441-8580, Japan.

N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and long-term depression (LTD) of signal transmission form neural circuits and thus are thought to underlie learning and memory. These mechanisms are mediated by AMPA receptor (AMPAR) trafficking in postsynaptic neurons. However, the regulatory mechanism of bidirectional plasticity at excitatory synapses remains unclear. Read More

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September 2020

Protease-activated receptor 1 (PAR1) inhibits synaptic NMDARs in mouse nigral dopaminergic neurons.

Pharmacol Res 2020 10 3;160:105185. Epub 2020 Sep 3.

Department of Experimental Neuroscience, IRCCS Fondazione Santa Lucia, Rome, Italy. Electronic address:

Protease-activated receptor 1 (PAR1) is a G protein-coupled receptor (GPCR), whose activation requires a proteolytic cleavage in the extracellular domain exposing a tethered ligand, which binds to the same receptor thus stimulating Gα-, Gα- and Gα proteins. PAR1, activated by serine proteases and matrix metalloproteases, plays multifaceted roles in neuroinflammation and neurodegeneration, in stroke, brain trauma, Alzheimer's diseases, and Parkinson's disease (PD). Substantia nigra pars compacta (SNpc) is among areas with highest PAR1 expression, but current evidence on its roles herein is restricted to mechanisms controlling dopaminergic (DAergic) neurons survival, with controversial data showing PAR1 either fostering or counteracting degeneration in PD models. Read More

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October 2020