106 results match your criteria enhancement ampar

Iridoids from Gardeniae fructus ameliorates depression by enhancing synaptic plasticity via AMPA receptor-mTOR signaling.

J Ethnopharmacol 2021 Mar 8;268:113665. Epub 2020 Dec 8.

School of Chinese Medicine & School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. Electronic address:

Ethnopharmacological Relevance: Gardeniae fructus is a traditional Chinese herb which exerts antidepressant effect. However, its effective constituent and potential mechanism are still unknown.

Aim Of The Study: To examine whether iridoids, a type of monoterpenoids from Gardeniae fructus (IGF), exerts antidepressant effect by enhancing synaptic plasticity via AMPA receptor-mTOR signaling. Read More

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Dopamine D1 and Glutamate Receptors Co-operate With Brain-Derived Neurotrophic Factor (BDNF) and TrkB to Modulate ERK Signaling in Adult Striatal Slices.

Front Cell Neurosci 2020 16;14:564106. Epub 2020 Nov 16.

Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, United Kingdom.

In the striatum, the input nucleus of the basal ganglia, the extracellular-signal-regulated kinase (ERK) pathway, necessary for various forms of behavioral plasticity, is triggered by the combined engagement of dopamine D1 and ionotropic glutamate receptors. In this study, we investigated the potential crosstalk between glutamatergic, dopaminergic, and brain-derived neurotrophic factor (BDNF)-TrkB inputs to ERK cascade by using an model of mouse striatal slices. Our results confirmed that the concomitant stimulation of D1 and glutamate receptors is necessary to activate ERK in striatal medium spiny neurons (MSNs). Read More

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November 2020

Restoration of Cingulate Long-Term Depression by Enhancing Non-apoptotic Caspase 3 Alleviates Peripheral Pain Hypersensitivity.

Cell Rep 2020 11;33(6):108369

Department of Neurobiology and Department of Anesthesiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, China; NHC and CAMS Key Laboratory of Medical Neurobiology, MOE Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Zhejiang, China. Electronic address:

Nerve injury in somatosensory pathways may lead to neuropathic pain, which affects the life quality of ∼8% of people. Long-term enhancement of excitatory synaptic transmission along somatosensory pathways contributes to neuropathic pain. Caspase 3 (Casp3) plays a non-apoptotic role in the hippocampus and regulates internalization of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits. Read More

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November 2020

Early life stress facilitates synapse premature unsilencing to enhance AMPA receptor function in the developing hippocampus.

J Neurophysiol 2020 09 12;124(3):815-821. Epub 2020 Aug 12.

Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada.

Chronic early life stress (ELS) increases vulnerability to psychopathologies and cognitive deficits in adulthood by disrupting the function of related neural circuits. However, whether this disruption emerges early in the developing brain remains largely unexplored. In the current study, using an established limited-bedding and nesting model of ELS in postnatal day (P)2-10 mice, we provide direct evidence that ELS caused early modification of hippocampal glutamatergic synapses in the developing brain. Read More

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September 2020

Acute application of extract enhanced AMPAR-mediated postsynaptic currents in rat entorhinal cortex.

J Integr Neurosci 2020 Jun;19(2):217-227

Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia, Jalan Hospital Universiti Sains Malaysia, 16150, Kubang Kerian, Kota Bharu, Kelantan, Malaysia.

is notable for its wide range of biological activities beneficial to human health, particularly its cognitive enhancement and neuroprotective effects. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors are ionotropic glutamate receptors mediating fast excitatory neurotransmission essential in long-term potentiation widely thought to be the cellular mechanism of learning and memory. The method of whole-cell patch-clamp was used to study the effect of the acute application of extract on the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated spontaneous excitatory postsynaptic currents in the entorhinal cortex of rat brain slices. Read More

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Transient appearance of Ca -permeable AMPA receptors is crucial for the production of repetitive LTP-induced synaptic enhancement (RISE) in cultured hippocampal slices.

Hippocampus 2020 07 22;30(7):763-769. Epub 2020 Apr 22.

Department of Neuroscience, Osaka University Graduate School of Frontier Biosciences, Osaka, Japan.

We have previously shown that repetitive induction of long-term potentiation (LTP) by glutamate (100 μM, 3 min, three times at 24-hr intervals) provoked long-lasting synaptic enhancement accompanied by synaptogenesis in rat hippocampal slice cultures, a phenomenon termed RISE (repetitive LTP-induced synaptic enhancement). Here, we examined the role of Ca -permeable (CP) AMPA receptors (AMPARs) in the establishment of RISE. We first found a component sensitive to the Joro-spider toxin (JSTX), a blocker of CP-AMPARs, in a field EPSP recorded from CA3-CA1 synapses at 2-3 days after stimulation, but this component was not found for 9-10 days. Read More

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BDNF Overexpression Enhances the Preconditioning Effect of Brief Episodes of Hypoxia, Promoting Survival of GABAergic Neurons.

Neurosci Bull 2020 Jul 27;36(7):733-760. Epub 2020 Mar 27.

Institute of Cell Biophysics of the Russian Academy of Sciences, Federal Research Center "Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences", Pushchino, Russia.

Hypoxia causes depression of synaptic plasticity, hyperexcitation of neuronal networks, and the death of specific populations of neurons. However, brief episodes of hypoxia can promote the adaptation of cells. Hypoxic preconditioning is well manifested in glutamatergic neurons, while this adaptive mechanism is virtually suppressed in GABAergic neurons. Read More

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Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex.

Aging (Albany NY) 2020 03 9;12(5):4299-4321. Epub 2020 Mar 9.

School of Biomedical Engineering, Tianjin Medical University, Tianjin, China.

Brain ischemia results from cardiac arrest, stroke or head trauma. The structural basis of rescuing the synaptic impairment and cortical dysfunctions induced in the stage of ischemic-reperfusion can occur if therapeutic interventions are applied in time, but the functional basis for this resilience remains elusive. Here, we explore the changes in cortical activity and a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) GluA1 subunit in spine (sGluA1) after transient ischemia-reperfusion for 28 days. Read More

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Subunit-Specific Augmentation of AMPA Receptor Ubiquitination by Phorbol Ester.

Cell Mol Neurobiol 2020 Oct 12;40(7):1213-1222. Epub 2020 Feb 12.

Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, QLD, 4072, Australia.

Excitatory neurotransmission relies on the precise targeting of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors to the neuronal plasma membrane. Activity-dependent ubiquitination of AMPA receptor (AMPAR) subunits sorts internalised receptors to late endosomes for degradation, which ultimately determines the number of AMPARs on neuronal membrane. Our recent study has demonstrated a functional cross-talk between the phosphorylation and ubiquitination of the GluA1 subunit in mammalian central neurons. Read More

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October 2020

Neuronal TDP-43 depletion affects activity-dependent plasticity.

Neurobiol Dis 2019 10 6;130:104499. Epub 2019 Jun 6.

Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland. Electronic address:

TAR DNA-binding protein 43 (TDP-43) is a hallmark of some neurodegenerative disorders, such as frontotemporal lobar degeneration and amyotrophic lateral sclerosis. TDP-43-related pathology is characterized by its abnormally phosphorylated and ubiquitinated aggregates. It is involved in many aspects of RNA processing, including mRNA splicing, transport, and translation. Read More

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October 2019

Exercise Prevents Memory Consolidation Defects Via Enhancing Prolactin Responsiveness of CA1 Neurons in Mice Under Chronic Stress.

Mol Neurobiol 2019 Sep 23;56(9):6609-6625. Epub 2019 Mar 23.

Department of Molecular Medicine and Tissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Mok-6-dong 911-1, Yangchun-Ku, Seoul, 158-710, South Korea.

We investigated the effects of regular exercise on chronic stress-induced memory consolidation impairment and its underlying mechanism. We focused on prolactin (PRL)-modulated calcium-permeable (CP)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPARs) in neurons in the CA1 stratum lacunosum-moleculare (SLM) area of the dorsal hippocampus. Regular exercise protected against memory retention defects and prevented dendritic retraction in apical distal segments of hippocampal CA1 neurons, as indicated by enhanced dendritic ramification, dendritic length, spine density, and synaptic protein levels following chronic stress. Read More

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September 2019

Seizure-Induced Potentiation of AMPA Receptor-Mediated Synaptic Transmission in the Entorhinal Cortex.

Front Cell Neurosci 2018 11;12:486. Epub 2018 Dec 11.

Laboratory of Molecular Mechanisms of Neural Interactions, Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, Saint Petersburg, Russia.

Excessive excitation is considered one of the key mechanisms underlying epileptic seizures. We investigated changes in the evoked postsynaptic responses of medial entorhinal cortex (ERC) pyramidal neurons by seizure-like events (SLEs), using the modified 4-aminopyridine (4-AP) model of epileptiform activity. Rat brain slices were perfused with pro-epileptic solution contained 4-AP and elevated potassium and reduced magnesium concentration. Read More

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December 2018

Shank and Zinc Mediate an AMPA Receptor Subunit Switch in Developing Neurons.

Front Mol Neurosci 2018 9;11:405. Epub 2018 Nov 9.

Department of Neurology & Neurological Sciences, School of Medicine, Stanford University, Stanford, CA, United States.

During development, pyramidal neurons undergo dynamic regulation of AMPA receptor (AMPAR) subunit composition and density to help drive synaptic plasticity and maturation. These normal developmental changes in AMPARs are particularly vulnerable to risk factors for Autism Spectrum Disorders (ASDs), which include loss or mutations of synaptic proteins and environmental insults, such as dietary zinc deficiency. Here, we show how Shank2 and Shank3 mediate a zinc-dependent regulation of AMPAR function and subunit switch from GluA2-lacking to GluA2-containing AMPARs. Read More

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November 2018

Visualization of Exo- and Endocytosis of AMPA Receptors During Hippocampal Synaptic Plasticity Around Postsynaptic-Like Membrane Formed on Glass Surface.

Tomoo Hirano

Front Cell Neurosci 2018 21;12:442. Epub 2018 Nov 21.

Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan.

Regulation of exo- and endocytosis of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor (AMPAR) plays a critical role in the expression of synaptic plasticity such as long-term potentiation (LTP) and long-term depression (LTD) at excitatory central synapses. Enhanced AMPAR exocytosis or endocytosis has been suggested to contribute to LTP or LTD, respectively. However, several unsettled fundamental questions have remained about AMPAR exo- and endocytosis in the basal condition and during synaptic plasticity: (1) Does the size of each exo- or endocytosis event, and/or do the frequencies of these events change during LTP or LTD? If they change, what are the time courses of the respective changes? (2) Where does the exo- or endocytosis preferentially occur in each condition: inside or in the vicinity of postsynaptic membrane, or in the extrasynaptic membrane? (3) Do different types of AMPAR, such as GluA1 homo-tetramer, GluA1/2 hetero-tetramer and GluA2/3 hetero-tetramer, show distinct exo- and endocytosis changes? To address these questions, we developed new methods to observe individual events of AMPAR exo- or endocytosis with a high signal to noise (SN) ratio in a culture preparation using total internal reflection fluorescence microscopy (TIRFM). Read More

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November 2018

Mechanisms of CPT1C-Dependent AMPAR Trafficking Enhancement.

Front Mol Neurosci 2018 8;11:275. Epub 2018 Aug 8.

Laboratori de Neurofisiologia, Departament de Biomedicina, Facultat de Medicina i Ciències de la Salut, Institut de Neurociències, Universitat de Barcelona, Barcelona, Spain.

In neurons, AMPA receptor (AMPAR) function depends essentially on their constituent components:the ion channel forming subunits and ion channel associated proteins. On the other hand, AMPAR trafficking is tightly regulated by a vast number of intracellular neuronal proteins that bind to AMPAR subunits. It has been recently shown that the interaction between the GluA1 subunit of AMPARs and carnitine palmitoyltransferase 1C (CPT1C), a novel protein partner of AMPARs, is important in modulating surface expression of these ionotropic glutamate receptors. Read More

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Suppression of AMPA Receptor Exocytosis Contributes to Hippocampal LTD.

J Neurosci 2018 06 21;38(24):5523-5537. Epub 2018 May 21.

Department of Biophysics, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan

The decrease in number of AMPA-type glutamate receptor (AMPAR) at excitatory synapses causes LTD, a cellular basis of learning and memory. The number of postsynaptic AMPARs is regulated by the balance of exocytosis and endocytosis, and enhanced endocytosis of AMPAR has been suggested to underlie the LTD expression. However, it remains unclear how endocytosis and exocytosis of AMPAR change during LTD. Read More

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Amyloid-β Induces AMPA Receptor Ubiquitination and Degradation in Primary Neurons and Human Brains of Alzheimer's Disease.

J Alzheimers Dis 2018 ;62(4):1789-1801

Department of Biology, Boston University, Boston, MA, USA.

As the primary mediator for synaptic transmission, AMPA receptors (AMPARs) are crucial for synaptic plasticity and higher brain functions. A downregulation of AMPAR expression has been indicated as one of the early pathological molecular alterations in Alzheimer's disease (AD), presumably via amyloid-β (Aβ). However, the molecular mechanisms leading to the loss of AMPARs remain less clear. Read More

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Δ-opioid receptor inhibition prevents remifentanil-induced post-operative hyperalgesia via regulating GluR1 trafficking and AMPA receptor function.

Exp Ther Med 2018 Feb 18;15(2):2140-2147. Epub 2017 Dec 18.

Department of Anesthesiology, The Second Hospital Affiliated to Tianjin Medical University, Tianjin 300042, P.R. China.

The interaction of remifentanil with glutamate systems has an important role in remifentanil-induced thermal and mechanical hyperalgesia. A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons. The present study demonstrated that δ opioid receptor (DOR) inhibition prevented thermal and mechanical hyperalgesia, which was induced by remifentanil infusion via attenuating GluR1 subunit trafficking and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) function in dorsal horn neurons. Read More

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February 2018

Glutamate receptor GluA1 subunit is implicated in capsaicin induced modulation of amygdala LTP but not LTD.

Learn Mem 2018 01 15;25(1):1-7. Epub 2017 Dec 15.

Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, CCM, CCO, 10117 Berlin, Germany.

Capsaicin has been shown to modulate synaptic plasticity in various brain regions including the amygdala. Whereas in the lateral amygdala the modulatory effect of capsaicin on long-term potentiation (LA-LTP) is mediated by TRPV1 channels, we have recently shown that capsaicin-induced enhancement of long term depression (LA-LTD) is mediated by TRPM1 receptors. However, the underlying mechanism by which capsaicin modulates synaptic plasticity is poorly understood. Read More

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January 2018

Loss of FMRP Impaired Hippocampal Long-Term Plasticity and Spatial Learning in Rats.

Front Mol Neurosci 2017 28;10:269. Epub 2017 Aug 28.

State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University-IDG/McGovern Institute for Brain Research, Peking UniversityBeijing, China.

Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by mutations in the gene that inactivate expression of the gene product, the fragile X mental retardation 1 protein (FMRP). In this study, we used clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) technology to generate knockout (KO) rats by disruption of the fourth exon of the gene. Western blotting analysis confirmed that the FMRP was absent from the brains of the KO rats ( ). Read More

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Hydroxynorketamine: Implications for the NMDA Receptor Hypothesis of Ketamine's Antidepressant Action.

Chronic Stress (Thousand Oaks) 2017 Jan-Dec;1. Epub 2017 Dec 12.

Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada.

The prevailing hypothesis of ketamine's unique antidepressant effects implicates N-methyl-d-aspartate receptor (NMDAR) inhibition-dependent enhancement of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated transmission, activation of intracellular signalling pathways and increased synaptogenesis. Recently, however, a seminal study by Zanos et al. directly challenged the NMDAR hypothesis of ketamine with the claim that an active ketamine metabolite, (2R,6R)-hydroxynorketamine, devoid of NMDAR binding properties or key side effects of its parent compound, is both necessary and sufficient for ketamine's antidepressant effects in rodents. Read More

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December 2017

D-Cycloserine Restores Experience-Dependent Neuroplasticity after Traumatic Brain Injury in the Developing Rat Brain.

J Neurotrauma 2017 04 23;34(8):1692-1702. Epub 2017 Jan 23.

1 Department of Neurosurgery, UCLA Brain Injury Research Center , Los Angeles, California.

Traumatic brain injury (TBI) in children can cause persisting cognitive and behavioral dysfunction, and inevitably raises concerns about lost potential in these injured youth. Lateral fluid percussion injury (FPI) in weanling rats pathologically affects hippocampal N-methyl-d-aspartate receptor (NMDAR)- and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated glutamatergic neurotransmission subacutely within the first post-injury week. FPI to weanling rats has also been shown to impair enriched-environment (EE) induced enhancement of Morris water maze (MWM) learning and memory in adulthood. Read More

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Nicotine-induced neuroplasticity counteracts the effect of schizophrenia-linked neuregulin 1 signaling on NMDAR function in the rat hippocampus.

Neuropharmacology 2017 02 23;113(Pt A):386-395. Epub 2016 Oct 23.

Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-4550, USA. Electronic address:

A high rate of heavy tobacco smoking among people with schizophrenia has been suggested to reflect self-medication and amelioration of cognitive dysfunction, a core feature of schizophrenia. NMDAR hypofunction is hypothesized to be a mechanism of cognitive dysfunction, and excessive schizophrenia-linked neuregulin 1 (NRG1) signaling through its receptor ErbB4 can suppress NMDAR function by preventing Src-mediated enhancement of NMDAR responses. Here we investigated whether chronic nicotine exposure in rats by subcutaneous injection of nicotine (0. Read More

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February 2017

Cross-regulation of Phosphodiesterase 1 and Phosphodiesterase 2 Activities Controls Dopamine-mediated Striatal α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptor Trafficking.

J Biol Chem 2016 10 7;291(44):23257-23267. Epub 2016 Sep 7.

From the Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029

Dopamine, a key striatal neuromodulator, increases synaptic strength by promoting surface insertion and/or retention of AMPA receptors (AMPARs). This process is mediated by the phosphorylation of the GluA1 subunit of AMPAR by cyclic nucleotide-dependent kinases, making cyclic nucleotide phosphodiesterases (PDEs) potential regulators of synaptic strength. In this study, we examined the role of phosphodiesterase 2 (PDE2), a medium spiny neuron-enriched and cGMP-activated PDE, in AMPAR trafficking. Read More

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October 2016

Integrated regulation of AMPA glutamate receptor phosphorylation in the striatum by dopamine and acetylcholine.

Neuropharmacology 2017 01 7;112(Pt A):57-65. Epub 2016 Apr 7.

Department of Basic Medical Science, School of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA; Department of Anesthesiology, School of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA; Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China. Electronic address:

Dopamine (DA) and acetylcholine (ACh) signals converge onto protein kinase A (PKA) in medium spiny neurons of the striatum to control cellular and synaptic activities of these neurons, although underlying molecular mechanisms are less clear. Here we measured phosphorylation of the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) at a PKA site (S845) as an indicator of AMPAR responses in adult rat brains in vivo to explore how DA and ACh interact to modulate AMPARs. We found that subtype-selective activation of DA D1 receptors (D1Rs), D2 receptors (D2Rs), or muscarinic M4 receptors (M4Rs) induced specific patterns of GluA1 S845 responses in the striatum. Read More

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January 2017

CaMKII Phosphorylation of TARPγ-8 Is a Mediator of LTP and Learning and Memory.

Neuron 2016 Oct 22;92(1):75-83. Epub 2016 Sep 22.

Department of Cellular and Molecular Physiology, Program in Cellular Neuroscience, Neurodegeneration, and Repair, Department of Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA; Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address:

Protein phosphorylation is an essential step for the expression of long-term potentiation (LTP), a long-lasting, activity-dependent strengthening of synaptic transmission widely regarded as a cellular mechanism underlying learning and memory. At the core of LTP is the synaptic insertion of AMPA receptors (AMPARs) triggered by the NMDA receptor-dependent activation of Ca/calmodulin-dependent protein kinase II (CaMKII). However, the CaMKII substrate that increases AMPAR-mediated transmission during LTP remains elusive. Read More

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October 2016

Antidepressant-like effects of long-term sarcosine treatment in rats with or without chronic unpredictable stress.

Behav Brain Res 2017 01 21;316:1-10. Epub 2016 Aug 21.

Department of Anatomy, China Medical University, Taichung, Taiwan. Electronic address:

Sarcosine, an N-methyl-d-aspartate receptor enhancer, can improve depression-like behavior in rodent models and depression in humans. We found that a single dose of sarcosine exerted antidepressant-like effects with rapid concomitant increases in the mammalian target of rapamycin (mTOR) signaling pathway activation and enhancement of α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor (AMPAR) membrane insertion. Sarcosine may play a crucial role in developing novel therapy for depression. Read More

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January 2017

Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function.

Biol Psychiatry 2016 11 7;80(9):671-681. Epub 2016 Apr 7.

Department ofAnesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee; Department ofPsychiatry, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address:

Background: Excitatory synaptic transmission in the nucleus accumbens (NAc) is a key biological substrate underlying behavioral responses to psychostimulants and susceptibility to relapse. Studies have demonstrated that cocaine induces changes in glutamatergic signaling at distinct inputs to the NAc. However, consequences of cocaine experience on synaptic transmission from the midline nuclei of the thalamus (mThal) to the NAc have yet to be reported. Read More

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November 2016

Overexpression of Protein Kinase Mζ in the Hippocampus Enhances Long-Term Potentiation and Long-Term Contextual But Not Cued Fear Memory in Rats.

J Neurosci 2016 Apr;36(15):4313-24

CNS Research and

Unlabelled: The persistently active protein kinase Mζ (PKMζ) has been found to be involved in the formation and maintenance of long-term memory. Most of the studies investigating PKMζ, however, have used either putatively unselective inhibitors or conventional knock-out animal models in which compensatory mechanisms may occur. Here, we overexpressed an active form of PKMζ in rat hippocampus, a structure highly involved in memory formation, and embedded in several neural networks. Read More

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Chemokine CCL2 enhances NMDA receptor-mediated excitatory postsynaptic current in rat hippocampal slices-a potential mechanism for HIV-1-associated neuropathy?

J Neuroimmune Pharmacol 2016 06 11;11(2):306-15. Epub 2016 Mar 11.

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA.

Human immunodeficiency virus type 1 (HIV-1)-infected mononuclear phagocytes (brain macrophages and microglial cells) release proinflammatory cytokines and chemokines. Elevated levels of chemokine CC motif ligand 2 (CCL2, known previously as monocyte chemoattractant protein-1) have been detected in serum and cerebrospinal fluid (CSF) of HIV-1-infected individuals and the raised CCL2 in the CSF correlates with HIV-1-associated neurocognitive disorders. To understand how elevated CCL2 induces HIV-1-associated neuropathy, we studied effects of CCL2 on excitatory postsynaptic current (EPSCs) in the CA1 region of rat hippocampal brain slices using whole-cell patch recording techniques. Read More

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