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Articoli di riviste sul tema "Glutamatergic post-synaptic pathway"

Autore: Grafiati

Pubblicato: 14 marzo 2023

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1

DAVIS, R. E. "Neurophysiology of glutamatergic signalling and anthelmintic action in Ascaris suum: pharmacological evidence for a kainate receptor." Parasitology 116, no. 5 (1998): 471–86. http://dx.doi.org/10.1017/s0031182098002467.

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Electrophysiological and pharmacological techniques were used to study glutamatergic signalling in the parasitic nematode, Ascaris suum. Glutamate or kainate injections into whole worms produced a paralysed quasi-static posture similar to the waveform in behaving worms. The DE2 motorneuron class is a primary target. Several glutamatergic substances produced pronounced conductance increases and depolarization in DE2; domoate and kainate were the most potent agonists tested. Glutamate responses and spontaneous excitatory post-synaptic potentials in DE2 were reversibly blocked in sodium-free sali

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2

Duric, Vanja, Mounira Banasr, Craig A. Stockmeier, et al. "Altered expression of synapse and glutamate related genes in post-mortem hippocampus of depressed subjects." International Journal of Neuropsychopharmacology 16, no. 1 (2013): 69–82. http://dx.doi.org/10.1017/s1461145712000016.

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Abstract Major depressive disorder (MDD) has been linked to changes in function and activity of the hippocampus, one of the central limbic regions involved in regulation of emotions and mood. The exact cellular and molecular mechanisms underlying hippocampal plasticity in response to stress are yet to be fully characterized. In this study, we examined the genetic profile of micro-dissected subfields of post-mortem hippocampus from subjects diagnosed with MDD and comparison subjects matched for sex, race and age. Gene expression profiles of the dentate gyrus and CA1 were assessed by 48K human H

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3

Choi, In-Ae, Ji Hee Yun, Ji-Hye Kim, Hahn Young Kim, Dong-Hee Choi, and Jongmin Lee. "Sequential Transcriptome Changes in the Penumbra after Ischemic Stroke." International Journal of Molecular Sciences 20, no. 24 (2019): 6349. http://dx.doi.org/10.3390/ijms20246349.

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To investigate the changes in the expression of specific genes that occur during the acute-to-chronic post-stroke phase, we identified differentially expressed genes (DEGs) between naive cortical tissues and peri-infarct tissues at 1, 4, and 8 weeks after photothrombotic stroke. The profiles of DEGs were subjected to the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene ontology analyses, followed by string analysis of the protein–protein interactions (PPI) of the products of these genes. We found 3771, 536, and 533 DEGs at 1, 4, and 8 weeks after stroke, respectively. A marked d

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4

Kreyden, Victoria A., Elly B. Mawi, Kristen M. Rush, and Jennifer R. Kowalski. "UBC-9 Acts in GABA Neurons to Control Neuromuscular Signaling in C. elegans." Neuroscience Insights 15 (January 2020): 263310552096279. http://dx.doi.org/10.1177/2633105520962792.

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Regulation of excitatory to inhibitory signaling balance is essential to nervous system health and is maintained by numerous enzyme systems that modulate the activity, localization, and abundance of synaptic proteins. SUMOylation is a key post-translational regulator of protein function in diverse cells, including neurons. There, its role in regulating synaptic transmission through pre- and postsynaptic effects has been shown primarily at glutamatergic central nervous system synapses, where the sole SUMO-conjugating enzyme Ubc9 is a critical player. However, whether Ubc9 functions globally at

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5

Leahy, Shannon N., Chunzhu Song, Dominic J. Vita, and Kendal Broadie. "FMRP activity and control of Csw/SHP2 translation regulate MAPK-dependent synaptic transmission." PLOS Biology 21, no. 1 (2023): e3001969. http://dx.doi.org/10.1371/journal.pbio.3001969.

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Noonan syndrome (NS) and NS with multiple lentigines (NSML) cognitive dysfunction are linked to SH2 domain-containing protein tyrosine phosphatase-2 (SHP2) gain-of-function (GoF) and loss-of-function (LoF), respectively. In Drosophila disease models, we find both SHP2 mutations from human patients and corkscrew (csw) homolog LoF/GoF elevate glutamatergic transmission. Cell-targeted RNAi and neurotransmitter release analyses reveal a presynaptic requirement. Consistently, all mutants exhibit reduced synaptic depression during high-frequency stimulation. Both LoF and GoF mutants also show impair

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6

Vanover, Kimberly, Steven Glass, Susan Kozauer, et al. "30 Lumateperone (ITI-007) for the Treatment of Schizophrenia: Overview of Placebo-Controlled Clinical Trials and an Open-label Safety Switching Study." CNS Spectrums 24, no. 1 (2019): 190–91. http://dx.doi.org/10.1017/s1092852919000245.

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AbstractBackgroundLumateperone is a first-in-class agent in development for schizophrenia that acts synergistically through serotonergic, dopaminergic and glutamatergic systems. Lumateperone is a potent 5-HT2A antagonist, a mesolimbic/mesocortical dopamine phosphoprotein modulator (DPPM) with pre-synaptic partial agonist and post-synaptic antagonist activity at D2, a glutamate GluN2B receptor phosphoprotein modulator with D1-dependent enhancement of both NMDA and AMPA currents via the mTOR protein pathway and an inhibitor of serotonin reuptake.MethodsLumateperone was evaluated in 3 controlled

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7

Rosenbrock, Holger, Katja Kroker, Birgit Stierstorfer, Scott Hobson, Roberto Arban, and Cornelia Dorner-Ciossek. "S31. ENHANCEMENT OF SYNAPTIC PLASTICITY BY COMBINATION OF PDE2 AND PDE9 INHIBITION PRESUMABLY VIA PRE- AND POST-SYNAPTIC MECHANISMS." Schizophrenia Bulletin 46, Supplement_1 (2020): S43. http://dx.doi.org/10.1093/schbul/sbaa031.097.

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Abstract Background Evidence from clinical and preclinical studies has led to the hypothesis that impaired glutamatergic transmission and NMDA receptor hypofunction play an important role in cognitive impairment associated with schizophrenia (CIAS). Second messenger pathways depending on cAMP and/or cGMP are key regulators of glutamatergic transmission and NMDA receptor related pathways. Therefore, the specific cyclic nucleotide phosphodiesterases (PDEs) PDE2 and PDE9, expressed in cognition relevant brain regions such as cortex and hippocampus, are putative targets for cognition enhancement i

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8

Colombo and Francolini. "Glutamate at the Vertebrate Neuromuscular Junction: From Modulation to Neurotransmission." Cells 8, no. 9 (2019): 996. http://dx.doi.org/10.3390/cells8090996.

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Although acetylcholine is the major neurotransmitter operating at the skeletal neuromuscular junction of many invertebrates and of vertebrates, glutamate participates in modulating cholinergic transmission and plastic changes in the last. Presynaptic terminals of neuromuscular junctions contain and release glutamate that contribute to the regulation of synaptic neurotransmission through its interaction with pre- and post-synaptic receptors activating downstream signaling pathways that tune synaptic efficacy and plasticity. During vertebrate development, the chemical nature of the neurotransmit

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9

Losada-Pérez, María, Mamen Hernández García-Moreno, Irene García-Ricote, and Sergio Casas-Tintó. "Synaptic components are required for glioblastoma progression in Drosophila." PLOS Genetics 18, no. 7 (2022): e1010329. http://dx.doi.org/10.1371/journal.pgen.1010329.

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Glioblastoma (GB) is the most aggressive, lethal and frequent primary brain tumor. It originates from glial cells and is characterized by rapid expansion through infiltration. GB cells interact with the microenvironment and healthy surrounding tissues, mostly neurons and vessels. GB cells project tumor microtubes (TMs) contact with neurons, and exchange signaling molecules related to Wingless/WNT, JNK, Insulin or Neuroligin-3 pathways. This cell to cell communication promotes GB expansion and neurodegeneration. Moreover, healthy neurons form glutamatergic functional synapses with GB cells whic

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10

Mawey, Feytie Magda, Azimatul Karimah, Erlyn Limoa, and Muhammad Nazmuddin. "Neuroinflammation in Schizophrenia." Jurnal Psikiatri Surabaya 10, no. 1 (2021): 1. http://dx.doi.org/10.20473/jps.v10i1.20871.

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Schizophrenia is a chronic debilitating mental illness. In many aspects, the neuropathology of schizophrenia is closely associated with neuroinflammation, especially microglial activation. Microglial hyperactivity, which is characterized by the predominant release of proinflammatory cytokines serves as the basis of the neuroinflammation hypothesis in schizophrenia. The enhanced inflammatory induce neuronal susceptibility to oxidative stress and trigger, glutamatergic synaptic dysregulation, especially in the mesolimbic and mesocortical pathways. Many in vitro studies, in vivo animal evidence,

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11

Martinez De La Cruz, Braulio, Robert Markus, Sunir Malla, et al. "Modifying the m6A brain methylome by ALKBH5-mediated demethylation: a new contender for synaptic tagging." Molecular Psychiatry 26, no. 12 (2021): 7141–53. http://dx.doi.org/10.1038/s41380-021-01282-z.

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AbstractSynaptic plasticity processes, which underlie learning and memory formation, require RNA to be translated local to synapses. The synaptic tagging hypothesis has previously been proposed to explain how mRNAs are available at specific activated synapses. However how RNA is regulated, and which transcripts are silenced or processed as part of the tagging process is still unknown. Modification of RNA by N6-methyladenosine (m6A/m) influences the cellular fate of mRNA. Here, by advanced microscopy, we showed that m6A demethylation by the eraser protein ALKBH5 occurs at active synaptic riboso

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12

Coletto, L. A., F. Ingegnoli, C. Cambria, et al. "POS0430 SYNOVIAL FLUID-DERIVED EXTRACELLULAR VESICLES FROM RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS MODULATE DIFFERENT HIPPOCAMPAL SYNAPTIC ACTIVITIES." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 469.2–470. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3188.

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BackgroundAccumulating evidence suggests that poor mental health is one of the most common comorbidities of both rheumatoid arthritis (RA) and osteoarthritis (OA) [1]. Even if underpinning RA and OA are different genetic, structural, mechanical, and immunologic pathways involved in their pathogenesis, poor mental health, and joint involvement are intertwined and negatively affect their mutual course by contributing to global disability. Thus, new insights into mechanisms that link these disorders are needed to identify new actionable biomarkers to drive more personalized therapeutic strategies

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13

Turitskaya, T. G., S. N. Lukashev, V. P. Lyashenko, and G. G. Sidorenko. "The features of summary background electric activity of the hypothalamus of rats under conditions of chronic caffeine alimentation." Regulatory Mechanisms in Biosystems 9, no. 3 (2018): 417–25. http://dx.doi.org/10.15421/021862.

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One of the factors of the environment which essentially shifts homeostasis is diets which contain caffeine. The aim of the study was to find out the basic characteristics of background electrical activity of trophotrophic and ergotrophic zones of the hypothalamus in conditions of chronic caffeine alimentation. Experiments were carried out on non-linear white male rats. The first group consisted of control animals (n = 22). The second group (n = 24) was represented by the animals that were given pure caffeine in an amount of 150 mg/kg/day with their meal. The registration on a electrohypothalam

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14

Chen, Chuyu, Giulia Soto, Vasin Dumrongprechachan, et al. "Pathway-specific dysregulation of striatal excitatory synapses by LRRK2 mutations." eLife 9 (October 2, 2020). http://dx.doi.org/10.7554/elife.58997.

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LRRK2 is a kinase expressed in striatal spiny projection neurons (SPNs), cells which lose dopaminergic input in Parkinson’s disease (PD). R1441C and G2019S are the most common pathogenic mutations of LRRK2. How these mutations alter the structure and function of individual synapses on direct and indirect pathway SPNs is unknown and may reveal pre-clinical changes in dopamine-recipient neurons that predispose toward disease. Here, R1441C and G2019S knock-in mice enabled thorough evaluation of dendritic spines and synapses on pathway-identified SPNs. Biochemical synaptic preparations and super-r

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15

Chen, Li-Jin, Jeng-Rung Chen, and Guo-Fang Tseng. "Modulation of striatal glutamatergic, dopaminergic and cholinergic neurotransmission pathways concomitant with motor disturbance in rats with kaolin-induced hydrocephalus." Fluids and Barriers of the CNS 19, no. 1 (2022). http://dx.doi.org/10.1186/s12987-022-00393-1.

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Abstract Background Hydrocephalus is characterized by abnormal accumulation of cerebrospinal fluid in the cerebral ventricles and causes motor impairments. The mechanisms underlying the motor changes remain elusive. Enlargement of ventricles compresses the striatum of the basal ganglia, a group of nuclei involved in the subcortical motor circuit. Here, we used a kaolin-injection juvenile rat model to explore the effects of acute and chronic hydrocephalus, 1 and 5 weeks post-treatment, respectively on the three major neurotransmission pathways (glutamatergic, dopaminergic and cholinergic) in th

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16

Narita, Minoru, Keisuke Hashimoto, Taku Amano, et al. "Post-synaptic action of morphine on glutamatergic neuronal transmission related to the descending antinociceptive pathway in the rat thalamus." Journal of Neurochemistry, November 12, 2007, 071115085713011—??? http://dx.doi.org/10.1111/j.1471-4159.2007.05059.x.

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17

Laszlo, Zsofia I., Nicole Hindley, Anna Sanchez Avila, et al. "Synaptic proteomics reveal distinct molecular signatures of cognitive change and C9ORF72 repeat expansion in the human ALS cortex." Acta Neuropathologica Communications 10, no. 1 (2022). http://dx.doi.org/10.1186/s40478-022-01455-z.

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AbstractIncreasing evidence suggests synaptic dysfunction is a central and possibly triggering factor in Amyotrophic Lateral Sclerosis (ALS). Despite this, we still know very little about the molecular profile of an ALS synapse. To address this gap, we designed a synaptic proteomics experiment to perform an unbiased assessment of the synaptic proteome in the ALS brain. We isolated synaptoneurosomes from fresh-frozen post-mortem human cortex (11 controls and 18 ALS) and stratified the ALS group based on cognitive profile (Edinburgh Cognitive and Behavioural ALS Screen (ECAS score)) and presence

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18

Chatterjee, Rounak, Janet L. Paluh, Souradeep Chowdhury, Soham Mondal, Arnab Raha, and Amitava Mukherjee. "SyNC, a Computationally Extensive and Realistic Neural Net to Identify Relative Impacts of Synaptopathy Mechanisms on Glutamatergic Neurons and Their Networks in Autism and Complex Neurological Disorders." Frontiers in Cellular Neuroscience 15 (July 20, 2021). http://dx.doi.org/10.3389/fncel.2021.674030.

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Synaptic function and experience-dependent plasticity across multiple synapses are dependent on the types of neurons interacting as well as the intricate mechanisms that operate at the molecular level of the synapse. To understand the complexity of information processing at synaptic networks will rely in part on effective computational models. Such models should also evaluate disruptions to synaptic function by multiple mechanisms. By co-development of algorithms alongside hardware, real time analysis metrics can be co-prioritized along with biological complexity. The hippocampus is implicated

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19

Pascual Cuadrado, Diego, Anna Wierczeiko, Charlotte Hewel, Susanne Gerber, and Beat Lutz. "Dichotomic Hippocampal Transcriptome After Glutamatergic vs. GABAergic Deletion of the Cannabinoid CB1 Receptor." Frontiers in Synaptic Neuroscience 13 (April 8, 2021). http://dx.doi.org/10.3389/fnsyn.2021.660718.

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Brain homeostasis is the dynamic equilibrium whereby physiological parameters are kept actively within a specific range. The homeostatic range is not fixed and may change throughout the individual's lifespan, or may be transiently modified in the presence of severe perturbations. The endocannabinoid system has emerged as a safeguard of homeostasis, e.g., it modulates neurotransmission and protects neurons from prolonged or excessively strong activation. We used genetically engineered mouse lines that lack the cannabinoid type-1 receptor (CB1) either in dorsal telencephalic glutamatergic or in

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Aponte-Santiago, Nicole A., and J. Troy Littleton. "Synaptic Properties and Plasticity Mechanisms of Invertebrate Tonic and Phasic Neurons." Frontiers in Physiology 11 (December 16, 2020). http://dx.doi.org/10.3389/fphys.2020.611982.

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Defining neuronal cell types and their associated biophysical and synaptic diversity has become an important goal in neuroscience as a mechanism to create comprehensive brain cell atlases in the post-genomic age. Beyond broad classification such as neurotransmitter expression, interneuron vs. pyramidal, sensory or motor, the field is still in the early stages of understanding closely related cell types. In both vertebrate and invertebrate nervous systems, one well-described distinction related to firing characteristics and synaptic release properties are tonic and phasic neuronal subtypes. In

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Aponte-Santiago, Nicole A., and J. Troy Littleton. "Synaptic Properties and Plasticity Mechanisms of Invertebrate Tonic and Phasic Neurons." Frontiers in Physiology 11 (December 16, 2020). http://dx.doi.org/10.3389/fphys.2020.611982.

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Abstract (sommario):

Defining neuronal cell types and their associated biophysical and synaptic diversity has become an important goal in neuroscience as a mechanism to create comprehensive brain cell atlases in the post-genomic age. Beyond broad classification such as neurotransmitter expression, interneuron vs. pyramidal, sensory or motor, the field is still in the early stages of understanding closely related cell types. In both vertebrate and invertebrate nervous systems, one well-described distinction related to firing characteristics and synaptic release properties are tonic and phasic neuronal subtypes. In

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Burlando, Bruno, Viviana Mucci, Cherylea J. Browne, et al. "Mal de Debarquement Syndrome explained by a vestibulo–cerebellar oscillator." Mathematical Medicine and Biology: A Journal of the IMA, December 5, 2022. http://dx.doi.org/10.1093/imammb/dqac016.

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Abstract Mal de Debarquement Syndrome (MdDS) is a puzzling central vestibular disorder characterized by a long-lasting perception of oscillatory postural instability that may occur after sea travels or flights. We have postulated that MdDS originates from the post-disembarking persistence of an adaptive internal oscillator consisting of a loop system, involving the right and left vestibular nuclei, and the Purkinje cells of the right and left flocculonodular cerebellar cortex, connected by GABAergic and glutamatergic fibers. We have formulated here a mathematical model of the vestibulo–cerebel

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Abraham, Joseph R., Nicholas Szoko, John Barnard, et al. "Proteomic Investigations of Autism Brain Identify Known and Novel Pathogenetic Processes." Scientific Reports 9, no. 1 (2019). http://dx.doi.org/10.1038/s41598-019-49533-y.

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Abstract Autism Spectrum Disorder (ASD) is a set of heterogeneous neurodevelopmental conditions defined by impairments in social communication and restricted, repetitive behaviors, interests or activities. Only a minority of ASD cases are determined to have a definitive etiology and the pathogenesis of most ASD is poorly understood. We hypothesized that a global analysis of the proteomes of human ASD vs. control brain, heretofore not done, would provide important data with which to better understand the underlying neurobiology of autism. In this study, we characterized the proteomes of two bra

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