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https://www.readbyqxmd.com/read/28453662/mglur5-tunes-ngf-trka-signaling-to-orient-spiny-stellate-neuron-dendrites-toward-thalamocortical-axons-during-whisker-barrel-map-formation
#1
Jui-Yen Huang, Hui-Chen Lu
Neurons receive and integrate synaptic inputs at their dendrites, thus dendritic patterning shapes neural connectivity and behavior. Aberrant dendritogenesis is present in neurodevelopmental disorders such as Down's syndrome and autism. Abnormal glutamatergic signaling has been observed in these diseases, as has dysfunction of the metabotropic glutamate receptor 5 (mGluR5). Deleting mGluR5 in cortical glutamatergic neurons disrupted their coordinated dendritic outgrowth toward thalamocortical axons and perturbed somatosensory circuits...
April 27, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/28449558/in-silicomodel-driven-assessment-of-the-effects-of-brain-derived-neurotrophic-factor-deficiency-on-glutamate-and-gamma-aminobutyric-acid-implications-for-understanding-schizophrenia-pathophysiology
#2
Rimjhim Agrawal, Sunil Vasu Kalmady, Ganesan Venkatasubramanian
Objective: Deficient brain-derived neurotrophic factor (BDNF) is one of the important mechanisms underlying the neuroplasticity abnormalities in schizophrenia. Aberration in BDNF signaling pathways directly or circuitously influences neurotransmitters like glutamate and gamma-aminobutyric acid (GABA). For the first time, this study attempts to construct and simulate the BDNF-neurotransmitter network in order to assess the effects of BDNF deficiency on glutamate and GABA. Methods: Using CellDesigner, we modeled BDNF interactions with calcium influx via N-methyl-D-aspartate receptor (NMDAR)- Calmodulin activation; synthesis of GABA via cell cycle regulators protein kinase B, glycogen synthase kinase and β-catenin; transportation of glutamate and GABA...
May 31, 2017: Clinical Psychopharmacology and Neuroscience: the Official Scientific Journal of the Korean College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28446243/targeting-metabotropic-glutamate-receptors-for-novel-treatments-of-schizophrenia
#3
REVIEW
James Maksymetz, Sean P Moran, P Jeffrey Conn
Support for the N-methyl-D-aspartate receptor (NMDAR) hypofunction hypothesis of schizophrenia has led to increasing focus on restoring proper glutamatergic signaling as an approach for treatment of this devastating disease. The ability of metabotropic glutamate (mGlu) receptors to modulate glutamatergic neurotransmission has thus attracted considerable attention for the development of novel antipsychotics. Consisting of eight subtypes classified into three groups based on sequence homology, signal transduction, and pharmacology, the mGlu receptors provide a wide range of targets to modulate NMDAR function as well as glutamate release...
April 26, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28445465/assembly-of-functionally-integrated-human-forebrain-spheroids
#4
Fikri Birey, Jimena Andersen, Christopher D Makinson, Saiful Islam, Wu Wei, Nina Huber, H Christina Fan, Kimberly R Cordes Metzler, Georgia Panagiotakos, Nicholas Thom, Nancy A O'Rourke, Lars M Steinmetz, Jonathan A Bernstein, Joachim Hallmayer, John R Huguenard, Sergiu P Paşca
The development of the nervous system involves a coordinated succession of events including the migration of GABAergic (γ-aminobutyric-acid-releasing) neurons from ventral to dorsal forebrain and their integration into cortical circuits. However, these interregional interactions have not yet been modelled with human cells. Here we generate three-dimensional spheroids from human pluripotent stem cells that resemble either the dorsal or ventral forebrain and contain cortical glutamatergic or GABAergic neurons...
April 26, 2017: Nature
https://www.readbyqxmd.com/read/28445148/pkc-and-camk-ii-inhibitions-coordinately-rescue-ischemia-induced-gabaergic-neuron-dysfunction
#5
Li Huang, Chun Wang, Shidi Zhao, Rongjing Ge, Sudong Guan, Jin-Hui Wang
Cerebral ischemia leads to neuronal death for stroke, in which the imbalance between glutamatergic neurons and GABAergic neurons toward neural excitotoxicity is presumably involved. GABAergic neurons are vulnerable to pathological factors and impaired in an early stage of ischemia. The rescue of GABAergic neurons is expected to be the strategy to reserve ischemic neuronal impairment. As protein kinase C (PKC) and calmodulin-dependent protein kinase II (CaMK-II) are activated during ischemia, we have investigated whether the inhibitions of these kinases rescue the ischemic impairment of cortical GABAergic neurons...
April 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/28444183/calcium-dysregulation-and-cdk5-atm-pathway-involved-in-a-mouse-model-of-fragile-x-associated-tremor-ataxia-syndrome
#6
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...
April 21, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28443506/catestain-a-master-regulator-of-cardiovascular-functions
#7
Sushil K Mahata, Malapaka Kiranmayi, Nitish R Mahapatra
Cardiovascular disease (CVD), the most common cause of death globally, accounts for ~30% of all deaths worldwide. Hypertension is a common contributor to morbidity and mortality from CVD. The plasma concentration of chromogranin A (CgA) is elevated in patients with CVD as well as patients with established human essential hypertension and heart failure (HF). In contrast, the plasma level of the CgA-derived peptide catestatin (CST) is diminished in human essential hypertension. Low conversion of CgA-to-CST has been associated with increased mortality in patients hospitalized with acute HF...
April 24, 2017: Current Medicinal Chemistry
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
#8
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...
April 22, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28438413/functional-redundancy-between-canonical-endocannabinoid-signaling-systems-in-the-modulation-of-anxiety
#9
Gaurav Bedse, Nolan D Hartley, Emily Neale, Andrew D Gaulden, Toni A Patrick, Philip J Kingsley, Md Jashim Uddin, Niels Plath, Lawrence J Marnett, Sachin Patel
BACKGROUND: Increasing the available repertoire of effective treatments for mood and anxiety disorders represents a critical unmet need. Pharmacological augmentation of endogenous cannabinoid (eCB) signaling has been suggested to represent a novel approach to the treatment of anxiety disorders; however, the functional interactions between two canonical eCB pathways mediated via anandamide (N-arachidonylethanolamine [AEA]) and 2-arachidonoylglycerol (2-AG) in the regulation of anxiety are not well understood...
March 15, 2017: Biological Psychiatry
https://www.readbyqxmd.com/read/28435052/neurovascular-neuroenergetic-coupling-axis-in-the-brain-master-regulation-by-nitric-oxide-and-consequences-in-aging-and-neurodegeneration
#10
REVIEW
Cátia F Lourenço, Ana Ledo, Rui M Barbosa, João Laranjinha
The strict energetic demands of the brain require that nutrient supply and usage be fine-tuned in accordance with the specific temporal and spatial patterns of ever-changing levels of neuronal activity. This is achieved by adjusting local cerebral blood flow (CBF) as a function of activity level - neurovascular coupling - and by changing how energy substrates are metabolized and shuttled amongst astrocytes and neurons - neuroenergetic coupling. Both activity-dependent increase of CBF and O2 and glucose utilization by active neural cells are inextricably linked, establishing a functional metabolic axis in the brain, the neurovascular-neuroenergetic coupling axis...
April 20, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28429885/intravenous-self-administration-of-benzydamine-a-non-steroidal-anti-inflammatory-drug-with-a-central-cannabinoidergic-mechanism-of-action
#11
Riccardo Avvisati, Maria Meringolo, Emiliana Stendardo, Elisa Malavasi, Silvia Marinelli, Aldo Badiani
Benzydamine (BZY) is a non-steroidal anti-inflammatory drug used for the topical treatment of inflammations of the oral and vaginal mucosae. Virtually nothing is known about the central pharmacological actions of BZY. Yet there are reports of voluntary systemic overdosage of BZY in drug addicts, resulting in a euphoric, hallucinatory state. In the present study, we investigated the reinforcing properties of BZY in a rat self-administration paradigm. We found that BZY has a powerful reinforcing effect and that this effect is greatly facilitated in animals that already had substance experience, having previously self-administered heroin and cocaine, indicating cross sensitization between BZY and other common drugs of abuse...
April 21, 2017: Addiction Biology
https://www.readbyqxmd.com/read/28429309/%C3%AE-ketoadipic-acid-and-%C3%AE-aminoadipic-acid-cause-disturbance-of-glutamatergic-neurotransmission-and-induction-of-oxidative-stress-in-vitro-in-brain-of-adolescent-rats
#12
Janaína Camacho da Silva, Alexandre Umpierrez Amaral, Cristiane Cecatto, Alessandro Wajner, Kálita Dos Santos Godoy, Rafael Teixeira Ribeiro, Aline de Mello Gonçalves, Ângela Zanatta, Mateus Struecker da Rosa, Samanta Oliveira Loureiro, Carmen Regla Vargas, Guilhian Leipnitz, Diogo Onofre Gomes de Souza, Moacir Wajner
Tissue accumulation of α-ketoadipic (KAA) and α-aminoadipic (AAA) acids is the biochemical hallmark of α-ketoadipic aciduria. This inborn error of metabolism is currently considered a biochemical phenotype with uncertain clinical significance. Considering that KAA and AAA are structurally similar to α-ketoglutarate and glutamate, respectively, we investigated the in vitro effects of these compounds on glutamatergic neurotransmission in the brain of adolescent rats. Bioenergetics and redox homeostasis were also investigated because they represent fundamental systems for brain development and functioning...
April 20, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28428223/glutamatergic-mechanisms-involved-in-bladder-overactivity-and-pudendal-neuromodulation-in-cats
#13
Jamie Uy, Michelle Yu, Xuewen Jiang, Cameron Jones, Bing Shen, Jicheng Wang, James R Roppolo, William C de Groat, Changfeng Tai
The involvement of ionotropic glutamate receptors in bladder overactivity and pudendal neuromodulation was determined in α-chloralose anesthetized cats by intravenously administering MK801 (a NMDA receptor antagonist) or CP465022 (an AMPA receptor antagonist). Infusion of 0.5% acetic acid (AA) into the bladder produced bladder overactivity. In the first group of 5 cats, bladder capacity was significantly (p<0.05) reduced to 55.3±10.0% of saline control by AA irritation. Pudendal nerve stimulation (PNS) significantly (p<0...
April 20, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28426966/assembly-of-excitatory-synapses-in-the-absence-of-glutamatergic-neurotransmission
#14
Richard Sando, Eric Bushong, Yongchuan Zhu, Min Huang, Camille Considine, Sebastien Phan, Suyeon Ju, Marco Uytiepo, Mark Ellisman, Anton Maximov
Synaptic excitation mediates a broad spectrum of structural changes in neural circuits across the brain. Here, we examine the morphologies, wiring, and architectures of single synapses of projection neurons in the murine hippocampus that developed in virtually complete absence of vesicular glutamate release. While these neurons had smaller dendritic trees and/or formed fewer contacts in specific hippocampal subfields, their stereotyped connectivity was largely preserved. Furthermore, loss of release did not disrupt the morphogenesis of presynaptic terminals and dendritic spines, suggesting that glutamatergic neurotransmission is unnecessary for synapse assembly and maintenance...
April 19, 2017: Neuron
https://www.readbyqxmd.com/read/28426965/formation-and-maintenance-of-functional-spines-in-the-absence-of-presynaptic-glutamate-release
#15
Albrecht Sigler, Won Chan Oh, Cordelia Imig, Bekir Altas, Hiroshi Kawabe, Benjamin H Cooper, Hyung-Bae Kwon, Jeong-Seop Rhee, Nils Brose
Dendritic spines are the major transmitter reception compartments of glutamatergic synapses in most principal neurons of the mammalian brain and play a key role in the function of nerve cell circuits. The formation of functional spine synapses is thought to be critically dependent on presynaptic glutamatergic signaling. By analyzing CA1 pyramidal neurons in mutant hippocampal slice cultures that are essentially devoid of presynaptic transmitter release, we demonstrate that the formation and maintenance of dendrites and functional spines are independent of synaptic glutamate release...
April 19, 2017: Neuron
https://www.readbyqxmd.com/read/28425701/the-effects-of-glutamate-receptor-activation-on-local-oxygen-changes
#16
Lindsay Walton, Nick G Boustead, Susan Carroll, R Mark Wightman
Glutamate is ubiquitous throughout the brain and serves as the primary excitatory neurotransmitter. Neurons require energy to fire, and energetic substrates (i.e., O2, glucose) are renewed via cerebral blood flow (CBF) to maintain metabolic homeostasis. Magnetic resonance brain functionality studies rely on the assumption that CBF and neuronal activity are coupled consistently throughout the brain; however, the origin of neuronal activity does not always coincide with signals indicative of energy consumption (e...
April 20, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28423185/functional-identification-of-activity-regulated-high-affinity-glutamine-transport-in-hippocampal-neurons-inhibited-by-riluzole
#17
Jeffrey D Erickson
Glutamine (Gln) is considered the preferred precursor for the neurotransmitter pool of glutamate (Glu), the major excitatory transmitter in the mammalian CNS. Here, an activity-regulated, high-affinity Gln transport system is described in developing and mature neuron-enriched hippocampal cultures that is potently inhibited by riluzole (IC50 1.3 +/- 0.5μM), an anti-glutamatergic drug, and is blocked by low concentrations of 2-(methylamino)isobutyrate (MeAIB), a system A transport inhibitor. K(+) -stimulated MeAIB transport displays an affinity (Km ) for MeAIB of 37 +/- 1...
April 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28422371/effects-of-m1-and-m4-activation-on-excitatory-synaptic-transmission-in-ca1
#18
Catherine Thorn, Michael Popiolek, Eda Stark, Jeremy Edgerton
Hippocampal networks are particularly susceptible to dysfunction in many neurodegenerative diseases and neuropsychiatric disorders including Alzheimer's disease, Lewy body dementia, and schizophrenia. CA1, a major output region of the hippocampus, receives glutamatergic input from both hippocampal CA3 and entorhinal cortex, via the Schaffer collateral (SC) and temporoammonic (TA) pathways, respectively. SC and TA inputs to CA1 are thought to be differentially involved in the retrieval of previously stored memories versus the encoding of novel information, and switching between these two crucial hippocampal functions is thought to critically depend on acetylcholine (ACh) acting at muscarinic receptors...
April 19, 2017: Hippocampus
https://www.readbyqxmd.com/read/28421605/cholinergic-glutamatergic-co-transmission-in-striatal-cholinergic-interneurons-new-mechanisms-regulating-striatal-computation
#19
REVIEW
Ornela Kljakic, Helena Janickova, Vania F Prado, Marco A M Prado
It is well established that neurons secrete neuropeptides and ATP with classical neurotransmitters; however, certain neuronal populations are also capable of releasing two classical neurotransmitters by a process named co-transmission. Although there has been progress in our understanding of the molecular mechanism underlying co-transmission, the individual regulation of neurotransmitter secretion and the functional significance of this neuronal 'bilingualism' is still unknown. Striatal cholinergic interneurons (CINs) have been shown to secrete glutamate (Glu) in addition to acetylcholine (ACh) and are recognized for their role in the regulation of striatal circuits and behavior...
April 18, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28421533/changes-in-the-prefrontal-glutamatergic-and-parvalbumin-systems-of-mice-exposed-to-unpredictable-chronic-stress
#20
Ryan Shepard, Laurence Coutellier
The prefrontal cortex (PFC) is highly sensitive to the effects of stress, a known risk factor of mood disorders including anxiety and depression. Abnormalities in PFC functioning have been well described in humans displaying stress-induced depressive symptoms, and hypoactivity of the PFC is now recognized to be a key feature of the depressed brain. However, little is known about the causes and mechanisms leading to this altered prefrontal functional activity in the context of stress-related mood disorders. We previously showed that unpredictable chronic mild stress (UCMS) in mice increases prefrontal expression of parvalbumin (PV), an activity-dependent calcium-binding albumin protein expressed in a specific subtype of GABAergic neurons, highlighting a potential mechanism through which chronic stress leads to hypofunction of the PFC...
April 18, 2017: Molecular Neurobiology
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