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https://www.readbyqxmd.com/read/29339535/functional-changes-of-ampa-responses-in-human-induced-pluripotent-stem-cell-derived-neural-progenitors-in-fragile-x-syndrome
#1
Venkat Swaroop Achuta, Tommi Möykkynen, Ulla-Kaisa Peteri, Giorgio Turconi, Claudio Rivera, Kari Keinänen, Maija L Castrén
Altered neuronal network formation and function involving dysregulated excitatory and inhibitory circuits are associated with fragile X syndrome (FXS). We examined functional maturation of the excitatory transmission system in FXS by investigating the response of FXS patient-derived neural progenitor cells to the glutamate analog (AMPA). Neural progenitors derived from induced pluripotent stem cell (iPSC) lines generated from boys with FXS had augmented intracellular Ca2+ responses to AMPA and kainate that were mediated by Ca2+-permeable AMPA receptors (CP-AMPARs) lacking the GluA2 subunit...
January 16, 2018: Science Signaling
https://www.readbyqxmd.com/read/29337145/interaction-of-dcf1-with-atp1b1-induces-impairment-in-astrocyte-structural-plasticity-via-the-p38-signaling-pathway
#2
Jiao Wang, Fangfang Zhou, Dong Wang, Jie Li, Dongfang Lu, Qian Li, Hong Zhou, Weihao Li, Qian Wang, Yiliu Wu, Jiang Xie, Tieqiao Wen
Astrocytes are known to regulate and support neuronal and synaptic functions. Changes in their size and morphology in mouse models result in mental retardation. However, the mechanism underlying these morphological changes remains unclear. In the present study, abnormal astrocyte morphology was found in the mouse brain following knockout of dendritic cell factor 1 (Dcf1). Immunoprecipitation-mass spectrometry (IP-Mass) identified that ATP1B1 is bound to DCF1, and co-immunoprecipitation and cell fluorescence further confirmed an interaction between these two proteins, with asparagine residue 266 of ATP1B1 being required for the interaction with DCF1...
January 12, 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29332416/-autoimmune-encephalitis-possibilities-in-the-laboratory-investigation
#3
Katalin Böröcz, Zsófia Hayden, Viktória Mészáros, Zsuzsanna Csizmadia, Kornélia Farkas, Zoltán Kellermayer, Péter Balogh, Ferenc Nagy, Tímea Berki
INTRODUCTION: The role of autoimmune responses against central nervous system (CNS) antigens in encephalitis presenting with non-classified neurologic or psychiatric symptoms has been appreciated in the past decade. Paraneoplastic limbic encephalitis has a poor prognosis and is most commonly associated with lung, ovarium, and testicular neoplasms, leading to immune reactions against intracellular antigens (anti-Hu/ANNA1, anti-Ri/ANNA2, anti-CV2/CRMP5 and anti-Ma2/Ta). In contrast, the recently described autoimmune encephalitis subtypes present with a broad spectrum of symptoms, respond to autoimmune therapies well and usually associate with autoantibodies against neuronal cell surface receptors (NMDAR, GABABR, AMPAR) or synaptic proteins (LGI1, CASPR2)...
January 2018: Orvosi Hetilap
https://www.readbyqxmd.com/read/29327271/-paraneoplastic-neurological-syndromes-a-current-summary
#4
REVIEW
D De Simoni, R Höftberger
BACKGROUND: Paraneoplastic neurological syndromes (PNNS) are remote effects of a tumor and mediated by an altered immune reaction. In the last ten years, the spectrum of PNNS has changed profoundly with the discovery of a new category of neurological diseases that are associated with antibodies against surface or synaptic antigens. In contrast to classical PNNS, patients with surface receptor autoimmunity are often highly responsive to immunotherapy. OBJECTIVES: This article provides an update on the most relevant PNNS, focusing on specific syndromes associated with antibodies against classical onconeuronal antigens as well as surface and synaptic proteins...
January 11, 2018: Der Internist
https://www.readbyqxmd.com/read/29317777/a-kinase-anchoring-protein-150-akap150-promotes-cocaine-reinstatement-by-increasing-ampa-receptor-transmission-in-the-accumbens-shell
#5
Leonardo A Guercio, Mackenzie E Hofmann, Sarah E Swinford-Jackson, Julia S Sigman, Mathieu E Wimmer, Mark L Dell'Acqua, Heath D Schmidt, R Christopher Pierce
Previous work indicated that activation of D1-like dopamine receptors (D1DRs) in the nucleus accumbens shell promoted cocaine seeking through a process involving the activation of PKA and GluA1-containing AMPA receptors (AMPARs). A-kinase anchoring proteins (AKAPs) localize PKA to AMPARs leading to enhanced phosphorylation of GluA1. AKAP150, the most well-characterized isoform, plays an important role in several forms of neuronal plasticity. However, its involvement in drug addiction has been minimally explored...
December 12, 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/29311141/a-unique-homeostatic-signaling-pathway-links-synaptic-inactivity-to-postsynaptic-mtorc1
#6
Fredrick E Henry, Xiao Wang, David Serrano, Amanda S Perez, Cynthia J L Carruthers, Edward L Stuenkel, Michael A Sutton
mTORC1-dependent translational control plays a key role in several enduring forms of synaptic plasticity such as long term potentiation (LTP) and mGluR-dependent long term depression. Recent evidence demonstrates an additional role in regulating synaptic homeostasis in response to inactivity, where dendritic mTORC1 serves to modulate presynaptic function via retrograde signaling. Presently, it is unclear if LTP and homeostatic plasticity utilize a common route to mTORC1-dependent signaling or if each engage mTORC1 through distinct pathways...
January 8, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29291424/enhanced-incentive-motivation-in-obesity-prone-rats-is-mediated-by-nac-core-cp-ampars
#7
Rifka C Derman, Carrie R Ferrario
Studies in humans suggest that stronger incentive motivational responses to Pavlovian food cues may drive over-consumption leading to and maintaining obesity, particularly in susceptible individuals. However, whether this enhanced incentive motivation emerges as a consequence of obesity or rather precedes obesity is unknown. Moreover, while human imaging studies have provided important information about differences in striatal responsiveness between susceptible and non-susceptible individuals, the neural mechanisms mediating these behavioral differences are unknown...
December 29, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29277782/oncolytic-properties-of-ampakines-in-vitro
#8
Daniel P Radin, Richard Purcell, Arnold S Lippa
BACKGROUND/AIM: The 5-year survival rate of glioblastoma (GBM) is ~10%, demonstrating that a new therapeutic modality for this cancer is desperately needed. Complicating the search for such a modality is that most large molecules cannot pass through the blood brain barrier, so molecules demonstrating efficacy in vitro may not be useful in vivo because they never reach the brain. Recently, the selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX) was identified as an effective agent in targeting GBM in vitro and in vivo by agonizing AMPA-glutamate receptors (AMPARs), eliciting massive calcium influx and mitochondrial calcium overload and apoptosis...
January 2018: Anticancer Research
https://www.readbyqxmd.com/read/29276473/ferric-chelate-reductase-1-like-protein-frrs1l-associates-with-dynein-vesicles-and-regulates-glutamatergic-synaptic-transmission
#9
Wenyan Han, Huiqing Wang, Jun Li, Shizhong Zhang, Wei Lu
In the brain, AMPA receptors (AMPARs)-mediated excitatory synaptic transmission is critically regulated by the receptor auxiliary subunits. Recent proteomic studies have identified that Ferric Chelate Reductase 1 Like protein (FRRS1L), whose mutations in human lead to epilepsy, choreoathetosis, and cognitive deficits, is present in native AMPAR complexes in the brain. Here we have characterized FRRS1L in both heterologous cells and in mouse neurons. We found that FRRS1L interacts with both GluA1 and GluA2 subunits of AMPARs, but does not form dimers/oligomers, in HEK cells...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29274366/vesicular-glutamate-transporter-1-vglut1-mediated-glutamate-release-and-membrane-glua1-activation-is-involved-in-the-rapid-antidepressant-like-effects-of-scopolamine-in-mice
#10
Hanjie Yu, Mengmeng Li, Dongsheng Zhou, Dan Lv, Qi Liao, Zhongze Lou, Mengxin Shen, Zhen Wang, Ming Li, Xiao Xiao, Yanhua Zhang, Chuang Wang
Emerging data have identified certain drugs such as scopolamine as rapidly acting antidepressants for major depressive disorder (MDD) that increase glutamate release and induce neurotrophic factors through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) activation in rodent models. However, little research has addressed the direct mechanisms of scopolamine on AMPAR activation or vesicular glutamate transporter 1 (VGLUT1)-mediated glutamate release in the prefrontal cortex (PFC) of mice...
December 20, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29250591/shank-proteins-differentially-regulate-synaptic-transmission
#11
Rebecca Shi, Patrick Redman, Dipanwita Ghose, Yan Liu, Xiaobai Ren, Lei J Ding, Mingna Liu, Kendrick J Jones, Weifeng Xu
Shank proteins, one of the principal scaffolds in the postsynaptic density (PSD) of the glutamatergic synapses, have been associated with autism spectrum disorders and neuropsychiatric diseases. However, it is not known whether different Shank family proteins have distinct functions in regulating synaptic transmission, and how they differ from other scaffold proteins in this aspect. Here, we investigate the role of Shanks in regulating glutamatergic synaptic transmission at rat hippocampal SC-CA1 synapses, using lentivirus-mediated knockdown and molecular replacement combined with dual whole-cell patch clamp in hippocampal slice culture...
November 2017: ENeuro
https://www.readbyqxmd.com/read/29248613/high-frequency-stimulation-induces-ltd-of-ampa-receptor-mediated-postsynaptic-responses-and-ltp-of-synaptically-evoked-firing-in-the-dorsolateral-striatum
#12
Olga Skiteva, Ning Yao, Mona Nouhi, Karima Chergui
In the striatum, long term potentiation (LTP) and long-term depression (LTD) of glutamatergic transmission are believed to underlie motor learning and are impaired in animal models of Parkinson's disease. High frequency stimulation (HFS) is often used to induce synaptic plasticity in the brain. In the striatum, the polarity of HFS-induced plasticity is influenced by the recording conditions, which can differ between various studies. Here, we examined the ability of HFS to induce synaptic plasticity in the dorsolateral striatum in the presence of extracellular Mg2+ ions, with no GABAA receptor blocker, and without membrane depolarization during HFS...
December 14, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/29246976/glutamate-receptor-glua1-subunit-is-implicated-in-capsaicin-induced-modulation-of-amygdala-ltp-but-not-ltd
#13
Christine Gebhardt, Doris Albrecht
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. In the present study, we investigate the modulatory effect of capsaicin on synaptic plasticity in mice lacking the AMPAR subunit GluA1...
January 2018: Learning & Memory
https://www.readbyqxmd.com/read/29241198/fam3a-protects-against-glutamate-induced-toxicity-by-preserving-calcium-homeostasis-in-differentiated-pc12-cells
#14
Qing Song, Wen-Li Gou, Yu-Liang Zou
BACKGROUND/AIMS: Stroke is the leading cause of adult disability, and glutamate-induced dysregulation of intracellular Ca2+ homeostasis is a key mechanism. FAM3A is the first member of the family with sequence similarity 3 (FAM3) gene family, and its biological function remains largely unknown. We have recently reported that FAM3A exerts protective effects against oxidative stress and mitochondrial dysfunction in HT22 cells. METHODS: Here, we investigated the protective effects of FAM3A using a glutamate-induced neuronal injury model in nerve growth factor (NGF)-differentiated PC12 cells...
December 12, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29237760/thorase-variants-are-associated-with-defects-in-glutamatergic-neurotransmission-that-can-be-rescued-by-perampanel
#15
George K E Umanah, Marco Pignatelli, Xiling Yin, Rong Chen, Joshua Crawford, Stewart Neifert, Leslie Scarffe, Adam A Behensky, Noah Guiberson, Melissa Chang, Erica Ma, Jin Wan Kim, Cibele C Castro, Xiaobo Mao, Li Chen, Shaida A Andrabi, Mikhail V Pletnikov, Ann E Pulver, Dimitrios Avramopoulos, Antonello Bonci, David Valle, Ted M Dawson, Valina L Dawson
The AAA+ adenosine triphosphatase (ATPase) Thorase plays a critical role in controlling synaptic plasticity by regulating the expression of surface α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Bidirectional sequencing of exons of ATAD1, the gene encoding Thorase, in a cohort of patients with schizophrenia and healthy controls revealed rare Thorase variants. These variants caused defects in glutamatergic signaling by impairing AMPAR internalization and recycling in mouse primary cortical neurons...
December 13, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/29233883/uncorking-ampa-receptors
#16
Caitlin Sedwick
New JGP study explains how auxiliary proteins relieve polyamine block of AMPARs.
December 12, 2017: Journal of General Physiology
https://www.readbyqxmd.com/read/29230056/the-c-terminal-tails-of-endogenous-glua1-and-glua2-differentially-contribute-to-hippocampal-synaptic-plasticity-and-learning
#17
Zikai Zhou, An Liu, Shuting Xia, Celeste Leung, Junxia Qi, Yanghong Meng, Wei Xie, Pojeong Park, Graham L Collingridge, Zhengping Jia
Long-term potentiation (LTP) and depression (LTD) at glutamatergic synapses are intensively investigated processes for understanding the synaptic basis for learning and memory, but the underlying molecular mechanisms remain poorly understood. We have made three mouse lines where the C-terminal domains (CTDs) of endogenous AMPA receptors (AMPARs), the principal mediators of fast excitatory synaptic transmission, are specifically exchanged. These mice display profound deficits in synaptic plasticity without any effects on basal synaptic transmission...
January 2018: Nature Neuroscience
https://www.readbyqxmd.com/read/29228686/dl-3n-butylphthalide-reduces-epileptiform-activity-through-glua2-lacking-calcium-permeable-ampars-in-epilepsy-models
#18
Qin Yang, Yi-Da Hu, Xue-Feng Wang, Fang-Shuo Zheng
Epilepsy is the most prevalent chronic neurological disorder, and its pathological mechanism indicates that an imbalance between excitatory and inhibitory neurotransmission leads to neuronal hyperexcitability. Previous studies have suggested that dl-3n-butylphthalide (NBP) regulates the excitatory neurotransmitter glutamate in the brains of epileptic mice, however, the mechanisms are unknown. We investigated behavioral and electrophysiological factors in rats using NBP. In an in vivo pentylenetetrazole (PTZ)-induced epileptic seizure animal model, NBP decreased the generalized tonic-clonic seizure (GTCS) severity...
November 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/29225271/clinical-relapse-of-anti-ampa-receptor-encephalitis-associated-with-recurrence-of-thymoma
#19
Tsubasa Omi, Makoto Kinoshita, Akira Nishikawa, Takahito Tomioka, Kenichi Ohmori, Kei Fukada, Hidenori Matsunaga
We report a rare case of anti-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) encephalitis presenting clinical relapse in association with recurrence of thymoma. Anti-AMPAR encephalitis is an autoimmune-mediated neurological disease, frequently accompanied by the presence of neoplasms, thus comprising the spectrum of paraneoplastic syndrome. A patient had been in remission for 34 months showed clinical relapse 3 months after the detection of recurrent thymoma. Clinical relapse of anti-AMPAR encephalitis after the recurrence of an initially detected neoplasm has not been previously reported...
December 8, 2017: Internal Medicine
https://www.readbyqxmd.com/read/29225042/endogenous-dopamine-and-endocannabinoid-signaling-mediate-cocaine-induced-reversal-of-ampar-synaptic-potentiation-in-the-nucleus-accumbens-shell
#20
Anna E Ingebretson, Matthew C Hearing, Ethan D Huffington, Mark J Thomas
Repeated exposure to drugs of abuse alters the structure and function of neural circuits mediating reward, generating maladaptive plasticity in circuits critical for motivated behavior. Within meso-corticolimbic dopamine circuitry, repeated exposure to cocaine induces progressive alterations in AMPAR-mediated glutamatergic synaptic transmission. During a 10-14 day period of abstinence from cocaine, AMPAR signaling is potentiated at synapses on nucleus accumbens (NAc) medium spiny neurons (MSNs), promoting a state of heightened synaptic excitability...
December 7, 2017: Neuropharmacology
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