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Letteratura scientifica selezionata sul tema "Glutamatergic post-synaptic pathway"

Autore: Grafiati

Pubblicato: 14 marzo 2023

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

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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Abstract (sommario):

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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Abstract (sommario):

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 (sommario):

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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Abstract (sommario):

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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Abstract (sommario):

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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Abstract (sommario):

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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