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Glutamatergic dysregulation

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https://www.readbyqxmd.com/read/28932183/plant-polyphenols-and-exendin-4-prevent-hyperactivity-and-tnf-%C3%AE-release-in-lps-treated-in-vitro-neuron-astrocyte-microglial-networks
#1
Francesca Gullo, Michela Ceriani, Alessia D'Aloia, Enzo Wanke, Andrew Constanti, Barbara Costa, Marzia Lecchi
Increasing evidence supports a decisive role for neuroinflammation in the neurodegenerative process of several central nervous system (CNS) disorders. Microglia are essential mediators of neuroinflammation and can regulate a broad spectrum of cellular responses by releasing reactive oxygen intermediates, nitric oxide, proteases, excitatory amino acids, and cytokines. We have recently shown that also in ex-vivo cortical networks of neurons, astrocytes and microglia, an increased level of tumor necrosis factor-alpha (TNF-α) was detected a few hours after exposure to the bacterial endotoxin lipopolysaccharide (LPS)...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28928363/an-autism-spectrum-disorder-related-de-novo-mutation-hotspot-discovered-in-the-gef1-domain-of-trio
#2
Anastasiia Sadybekov, Chen Tian, Cosimo Arnesano, Vsevolod Katritch, Bruce E Herring
The Rho guanine nucleotide exchange factor (RhoGEF) Trio promotes actin polymerization by directly activating the small GTPase Rac1. Recent studies suggest that autism spectrum disorder (ASD)-related behavioral phenotypes in animal models of ASD can be produced by dysregulation of Rac1's control of actin polymerization at glutamatergic synapses. Here, in humans, we discover a large cluster of ASD-related de novo mutations in Trio's Rac1 activating domain, GEF1. Our study reveals that these mutations produce either hypofunctional or hyperfunctional forms of Trio in rodent neurons in vitro...
September 19, 2017: Nature Communications
https://www.readbyqxmd.com/read/28924227/implication-of-the-glutamate-cystine-antiporter-xct-in-schizophrenia-cases-linked-to-impaired-gsh-synthesis
#3
M Fournier, A Monin, C Ferrari, P S Baumann, P Conus, K Do
xCT is the specific chain of the cystine/glutamate antiporter, which is widely reported to support anti-oxidant defenses in vivo. xCT is therefore at the crossroads between two processes that are involved in schizophrenia: oxidative stress and glutamatergic neurotransmission. But data from human studies implicating xCT in the illness and clarifying the upstream mechanisms of xCT imbalance are still scarce. Low glutathione (GSH) levels and genetic risk in GCLC (Glutamate-Cysteine Ligase Catalytic subunit), the gene of limiting synthesizing enzyme for GSH, are both associated with schizophrenia...
September 18, 2017: NPJ Schizophrenia
https://www.readbyqxmd.com/read/28820053/neurobiological-mechanisms-of-stress-resilience-and-implications-for-the-aged-population
#4
Charlène Faye, Josephine C Mcgowan, Christine A Denny, Denis J David
Stress is a common reaction to an environmental adversity, but a dysregulation of the stress response can lead to psychiatric illnesses such as major depressive disorder (MDD), post-traumatic stress disorder (PTSD), and anxiety disorders. Yet, not all individuals exposed to stress will develop psychiatric disorders; those with enhanced stress resilience mechanisms have the ability to adapt successfully to stress without developing persistent psychopathology. Notably, the potential to enhance stress resilience in at-risk populations may prevent the onset of stress-induced psychiatric disorders...
August 17, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28800512/metabotropic-glutamate-receptors-as-emerging-research-targets-in-bipolar-disorder
#5
REVIEW
Caren J Blacker, Charles P Lewis, Mark A Frye, Marin Veldic
Glutamatergic dysregulation is implicated in the neuropathology of bipolar disorder (BD). There is increasing interest in investigating the role of metabotropic glutamate receptors (mGluRs) in BD and as a target for treatment intervention. Bipolar mGluR studies (published January 1992-April 2016) were identified via PubMed, Embase, Web of Science, and Scopus. Full-text screening, data extraction, and quality appraisal were conducted in duplicate, with strict inclusion and exclusion criteria. The initial literature search for mGluRs in BD, including non-bipolar mood disorders and primary psychotic disorders, identified 1544 articles...
July 31, 2017: Psychiatry Research
https://www.readbyqxmd.com/read/28796815/effect-of-teriflunomide-on-cortex-basal-ganglia-thalamus-cxbgth-circuit-glutamatergic-dysregulation-in-the-theiler-s-murine-encephalomyelitis-virus-mouse-model-of-multiple-sclerosis
#6
Claire M Modica, Ferdinand Schweser, Michelle L Sudyn, Nicola Bertolino, Marilena Preda, Paul Polak, Danielle M Siebert, Jacqueline C Krawiecki, Michele Sveinsson, Jesper Hagemeier, Michael G Dwyer, Suyog Pol, Robert Zivadinov
BACKGROUND: Pathology of gray matter is associated with development of physical and cognitive disability in patients with multiple sclerosis. In particular, glutamatergic dysregulation in the cortex-basal ganglia-thalamus (CxBGTh) circuit could be associated with decline in these behaviors. OBJECTIVES: To investigate the effect of an immunomodulatory therapy (teriflunomide, Aubagio®) on changes of the CxBGTh loop in the Theiler's Murine Encephalomyelitis Virus, (TMEV) mouse model of MS...
2017: PloS One
https://www.readbyqxmd.com/read/28738353/inflammation-effects-on-glutamate-as-a-pathway-to-neuroprogression-in-mood-disorders
#7
Ebrahim Haroon, Andrew H Miller
Neuroprogression is a term used to describe worsening psychopathology, poor treatment response, and declining cognitive and functional outcomes among patients with chronic mental disorders. Chronic inflammatory activation and glutamate-mediated excitotoxicity are two key etiological factors implicated in the development of neuroprogression. In this chapter, we hypothesize that the association between chronic inflammatory activation, neuroprogression, and glutamate dysregulation might be mediated by glial dysfunction...
2017: Modern Trends in Pharmacopsychiatry
https://www.readbyqxmd.com/read/28709906/effects-of-feeding-time-on-daily-rhythms-of-neuropeptide-and-clock-gene-expression-in-the-rat-hypothalamus
#8
Dawei Wang, Anne-Loes Opperhuizen, Jane Reznick, Nigel Turner, Yan Su, Gregory J Cooney, Andries Kalsbeek
Shiftworkers are exposed to several adverse health conditions, one being eating at night. Food consumption at an unnatural time-of-day is thought to be one of the main factors responsible for the increased risk of developing metabolic diseases, such as obesity and diabetes mellitus. The underlying mechanism is considered to include disruption of the circadian organization of physiology, leading to disruption of metabolism. When food is consumed at night, the hypothalamus, a brain region central to homeostasis, receives contradicting input from the central clock and the systemic circulation...
July 11, 2017: Brain Research
https://www.readbyqxmd.com/read/28683776/trpa1-channels-promote-astrocytic-ca-2-hyperactivity-and-synaptic-dysfunction-mediated-by-oligomeric-forms-of-amyloid-%C3%AE-peptide
#9
Anthony Bosson, Adrien Paumier, Sylvie Boisseau, Muriel Jacquier-Sarlin, Alain Buisson, Mireille Albrieux
BACKGROUND: Excessive synaptic loss is thought to be one of the earliest events in Alzheimer's disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes contribute to functional changes observed during synaptic plasticity and play a major role in synaptic dysfunction but astrocytes behavior and involvement in early phases of AD remained largely undefined. METHODS: We measure astrocytic calcium activity in mouse CA1 hippocampus stratum radiatum in both the global astrocytic population and at a single cell level, focusing in the highly compartmentalized astrocytic arbor...
July 6, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28676016/resilience-dysregulation-in-major-depressive-disorder-focus-on-glutamatergic-imbalance-and-microglial-activation
#10
Gislaine Z Réus, Airam B de Moura, Ritele H Silva, Wilson R Resende, João Quevedo
Many studies have been shown an important role of glutamatergic system as well microglial activation in the pathophysiology of major depressive disorder (MDD). Experimental and clinical data suggest that attenuation of N-methyl-D-aspartate (NMDA) receptor function exerts antidepressant effects. Glutamatergic system is involved with memory establishment and function, and it regulates plasticity in the brain. Microglial cells play pivotal role to the brain functions; however, under chronic inflammation status microglial could be turn activated and increase the pro-inflammatory cytokines...
July 3, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28676011/resilience-dysregulation-in-major-depressive-disorder-focus-on-glutamatergic-imbalance-and-microglial-activation
#11
Gislaine Z Réus, Airam B de Moura, Ritele H Silva, Wilson R Resende, João Quevedo
Many studies have been shown an important role of glutamatergic system as well microglial activation in the pathophysiology of major depressive disorder (MDD). Experimental and clinical data suggest that attenuation of N-methyl-D-aspartate (NMDA) receptor function exerts antidepressant effects. Glutamatergic system is involved with memory establishment and function, and it regulates plasticity in the brain. Microglial cells play pivotal role to the brain functions; however, under chronic inflammation status microglial could be turn activated and increase the pro-inflammatory cytokines...
June 30, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28622282/towards-a-neurobiological-understanding-of-alexithymia
#12
REVIEW
Nicolás Meza-Concha, Marcelo Arancibia, Felicia Salas, Rosa Behar, Germán Salas, Hernán Silva, Rocío Escobar
Although the specialized literature on the etiology of alexithymia is controversial, neurobiological research has shown relevant advances. The aim of this review is to analyze the available evidence regarding the neurophysiological bases of alexithymia. A comprehensive review of available articles from Medline/PubMed, EBSCO and SciELO was conducted. Previously, alexithymia was linked to a reduced interhemispheric brain connection. From a childhood traumatic perspective, the right prefrontal cortex and the default mode network would experience alterations, first hypermetabolic (dopaminergic and glutamatergic dysregulation) and then hypometabolic-dissociative (serotonergic and opioid dysregulation), resulting in a distorted interoceptive and emotional awareness...
May 29, 2017: Medwave
https://www.readbyqxmd.com/read/28605494/glutamate-transport-a-new-bench-to-bedside-mechanism-for-treating-drug-abuse
#13
Sade Spencer, Peter W Kalivas
Drug addiction has often been described as a "hijacking" of the brain circuits involved in learning and memory. Glutamate is the principal excitatory neurotransmitter in the brain, and its contribution to synaptic plasticity and learning processes is well established in animal models. Likewise, over the past twenty years the addiction field has ascribed a critical role for glutamatergic transmission in the development of addiction. Chronic drug use produces enduring neuroadaptations in corticostriatal projections that are believed to contribute to a maladaptive deficit in inhibitory control over behavior...
June 12, 2017: International Journal of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28580666/connexins-and-pannexins-at-the-junction-of-neuro-glial-homeostasis-disease
#14
REVIEW
Andrew S Lapato, Seema K Tiwari-Woodruff
In the central nervous system (CNS), connexin (Cx)s and pannexin (Panx)s are an integral component of homeostatic neuronal excitability and synaptic plasticity. Neuronal Cx gap junctions form electrical synapses across biochemically similar GABAergic networks, allowing rapid and extensive inhibition in response to principle neuron excitation. Glial Cx gap junctions link astrocytes and oligodendrocytes in the pan-glial network that is responsible for removing excitotoxic ions and metabolites. In addition, glial gap junctions help constrain excessive excitatory activity in neurons and facilitate astrocyte Ca(2+) slow wave propagation...
June 5, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28540422/loss-and-remodeling-of-striatal-dendritic-spines-in-parkinson-s-disease-from-homeostasis-to-maladaptive-plasticity
#15
REVIEW
Rosa M Villalba, Yoland Smith
In Parkinson's disease (PD) patients and animal models of PD, the progressive degeneration of the nigrostriatal dopamine (DA) projection leads to two major changes in the morphology of striatal projection neurons (SPNs), i.e., a profound loss of dendritic spines and the remodeling of axospinous glutamatergic synapses. Striatal spine loss is an early event tightly associated with the extent of striatal DA denervation, but not the severity of parkinsonian motor symptoms, suggesting that striatal spine pruning might be a form of homeostatic plasticity that compensates for the loss of striatal DA innervation and the resulting dysregulation of corticostriatal glutamatergic transmission...
May 24, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28444183/calcium-dysregulation-and-cdk5-atm-pathway-involved-in-a-mouse-model-of-fragile-x-associated-tremor-ataxia-syndrome
#16
Gaëlle Robin, José R López, Glenda M Espinal, Susan Hulsizer, Paul J Hagerman, Isaac N Pessah
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurological disorder that affects premutation carriers with 55-200 CGG-expansion repeats (preCGG) in FMR1, presenting with early alterations in neuronal network formation and function that precede neurodegeneration. Whether intranuclear inclusions containing DNA damage response (DDR) proteins are causally linked to abnormal synaptic function, neuronal growth and survival are unknown. In a mouse that harbors a premutation CGG expansion (preCGG), cortical and hippocampal FMRP expression is moderately reduced from birth through adulthood, with greater FMRP reductions in the soma than in the neurite, despite several-fold elevation of Fmr1 mRNA levels...
July 15, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28442364/effects-of-repeated-cocaine-exposure-and-withdrawal-on-voluntary-ethanol-drinking-and-the-expression-of-glial-glutamate-transporters-in-mesocorticolimbic-system-of-p-rats
#17
Alaa M Hammad, Yusuf S Althobaiti, Sujan C Das, Youssef Sari
Glutamatergic neurotransmission within the brain's reward circuits plays a major role in the reinforcing properties of both ethanol and cocaine. Glutamate homeostasis is regulated by several glutamate transporters, including glutamate transporter type 1 (GLT-1), cystine/glutamate transporter (xCT), and glutamate aspartate transporter (GLAST). Cocaine exposure has been shown to induce a dysregulation in glutamate homeostasis and a decrease in the expression of GLT-1 and xCT in the nucleus accumbens (NAc). In this study, alcohol preferring (P) rats were exposed to free-choice of ethanol (15% and 30%) and/or water for five weeks...
July 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28416811/gene-deficiency-and-pharmacological-inhibition-of-caspase-1-confers-resilience-to-chronic-social-defeat-stress-via-regulating-the-stability-of-surface-ampars
#18
M-X Li, H-L Zheng, Y Luo, J-G He, W Wang, J Han, L Zhang, X Wang, L Ni, H-Y Zhou, Z-L Hu, P-F Wu, Y Jin, L-H Long, H Zhang, G Hu, J-G Chen, F Wang
Both inflammatory processes and glutamatergic systems have been implicated in the pathophysiology of mood-related disorders. However, the role of caspase-1, a classic inflammatory caspase, in behavioral responses to chronic stress remains largely unknown. To address this issue, we examined the effects and underlying mechanisms of caspase-1 on preclinical murine models of depression. We found that loss of caspase-1 expression in Caspase-1(-/-) knockout mice alleviated chronic stress-induced depression-like behaviors, whereas overexpression of caspase-1 in the hippocampus of wild-type (WT) mice was sufficient to induce depression- and anxiety-like behaviors...
April 18, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28412922/abnormalities-in-kynurenine-pathway-metabolism-in-treatment-resistant-depression-and-suicidality-a-systematic-review
#19
Gianluca Serafini, Giulia Adavastro, Giovanna Canepa, Laura Capobianco, Claudia Conigliaro, Federica Pittaluga, Martino Belvederi Murri, Alessandro Valchera, Domenico De Berardis, Maurizio Pompili, Daniel Lindqvist, Lena Brundin, Mario Amore
Treatment resistant depression (TRD) and suicidal behavior are among the most important public health problems and are commonly associated with significant disability and psychosocial impairment. Although there have been recent advances in identifying neurobiological correlates of these complex conditions, their pathophysiology still remains unclear. Although the recent advances concerning the neurobiological determinants underlying these complex conditions, their pathophysiology still remains unclear. Compared to non-suicidal subjects, higher mean concentrations of inflammatory mediators have been found in both the periphery and brain of individuals at risk for suicide...
April 13, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28363984/blood-pressure-regulation-by-the-rostral-ventrolateral-medulla-in-conscious-rats-effects-of-hypoxia-hypercapnia-baroreceptor-denervation-and-anesthesia
#20
Ian C Wenker, Chikara Abe, Kenneth E Viar, Daniel S Stornetta, Ruth L Stornetta, Patrice G Guyenet
Current understanding of the contribution of C1 neurons to blood pressure (BP) regulation derives predominantly from experiments performed in anesthetized animals or reduced ex vivo preparations. Here, we use ArchaerhodopsinT3.0 (ArchT) loss-of-function optogenetics to explore BP regulation by C1 neurons in intact, unanesthetized rats. Using a lentivirus that expresses ArchT under the Phox2b-activated promoter PRSx8 (PRSx8-ArchT), ∼65% of transduced neurons were C1 (balance retrotrapezoid nucleus, RTN). Other rats received CaMKII-ArchT3...
April 26, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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