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Showing 1-30 of 96 results for "K0250" within Papers
Seena S Mathew et al.
Neuropharmacology, 55(1), 106-116 (2008-05-30)
We examined the mechanisms of kainate (KA) induced modulation of GABA release in rat prefrontal cortex. Pharmacologically isolated IPSCs were recorded from visually identified layer II/III pyramidal cells using whole-cell patch clamp techniques. KA produced an increase in evoked IPSC
Hume Stroud et al.
Neuron, 107(5), 874-890 (2020-06-27)
The maturation of the mammalian brain occurs after birth, and this stage of neuronal development is frequently impaired in neurological disorders, such as autism and schizophrenia. However, the mechanisms that regulate postnatal brain maturation are poorly defined. By purifying neuronal
Ritchie Chen et al.
Nature biotechnology, 39(2), 161-164 (2020-10-07)
Achieving temporally precise, noninvasive control over specific neural cell types in the deep brain would advance the study of nervous system function. Here we use the potent channelrhodopsin ChRmine to achieve transcranial photoactivation of defined neural circuits, including midbrain and
S-allyl L-cysteine protects the retina against kainate excitotoxicity in the rat.
Chao HM, Chen IL, and Liu JH
American Journal of Chinese Medicine, 42(3), 693-708 (2014)
Martina Di Nunzio et al.
Epilepsia, 62(8), 1931-1945 (2021-06-16)
Microgliosis occurs in animal models of acquired epilepsy and in patients. It includes cell proliferation that is associated with seizure frequency and decreased neuronal cells in human epilepsy. The role of microglia proliferation in the development of acquired epilepsy is
David G Nicholls et al.
Cell calcium, 34(4-5), 407-424 (2003-08-12)
The mitochondrion has moved to the center stage in the drama of the life and death of the neuron. The mitochondrial membrane potential controls the ability of the organelle to generate ATP, generate reactive oxygen species and sequester Ca(2+) entering
Zhenggang Wu et al.
Cytotechnology, 809-818 (2019-06-28)
To determine the function of miR-206 in epilepsy. Epileptic rat model was established by intra-amygdala injection of kainic acid (KA). Expression levels of miR-206, C-C Motif Chemokine Ligand 2 (CCL2) and interleukin-1β (Il-1β) in hippocampus tissues was measured by reverse
Kif Liakath-Ali et al.
Frontiers in molecular neuroscience, 14, 659681-659681 (2021-03-27)
Neurexins are presynaptic cell-adhesion molecules essential for synaptic function that are expressed in thousands of alternatively spliced isoforms. Recent studies suggested that alternative splicing at splice site 4 (SS4) of Nrxn1 is tightly regulated by an activity-dependent mechanism. Given that
Emily T Doisy et al.
Epilepsia, 56(4), 626-635 (2015-03-11)
Aberrations in brain development may lead to dysplastic structures such as periventricular nodules. Although these abnormal collections of neurons are often associated with difficult-to-control seizure activity, there is little consensus regarding the epileptogenicity of the nodules themselves. Because one common
Mike O Karl et al.
Methods in molecular biology (Clifton, N.J.), 884, 213-227 (2012-06-13)
Retinal regeneration has been studied for decades in nonmammalian species. From these studies, we learned that retinal Müller glia are a potential source of neuronal regeneration by de novo neurogenesis. Although spontaneous regeneration in mammals is absent after retinal damage
Seungjoon Kim et al.
Cell reports, 36(3), 109417-109417 (2021-07-22)
Activity-dependent GABAergic synapse plasticity is important for normal brain functions, but the underlying molecular mechanisms remain incompletely understood. Here, we show that Npas4 (neuronal PAS-domain protein 4) transcriptionally regulates the expression of IQSEC3, a GABAergic synapse-specific guanine nucleotide-exchange factor for
Jason C You et al.
PloS one, 15(5), e0232241-e0232241 (2020-05-15)
Under physiologic conditions, the dentate gyrus (DG) exhibits exceptionally low levels of activity compared to other brain regions. A sparse activation pattern is observed even when the DG is engaged to process new information; for example, only ~1-3% of neurons
D Schmitz et al.
Proceedings of the National Academy of Sciences of the United States of America, 98(20), 11003-11008 (2001-09-27)
Hippocampal mossy fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present
Deborah J Mi et al.
Neurobiology of aging, 71, 241-254 (2018-09-02)
Ascorbate (vitamin C) is critical as a first line of defense antioxidant within the brain, and specifically within the synapse. Ascorbate is released by astrocytes during glutamate clearance and disruption of this exchange mechanism may be critical in mediating glutamate
Jianping Si et al.
Experimental and therapeutic medicine, 20(6), 177-177 (2020-10-27)
The aim of the present study was to explore the potential anticonvulsant effects of β-hydroxybutyrate (BHB) in a kainic acid (KA)-induced rat epilepsy model. The KA-induced rat seizure model was established and BHB was administrated intraperitoneally at a dose of
Ting Chen et al.
Brain research bulletin, 144, 187-193 (2018-11-14)
Temporal lobe epilepsy (TLE) with hippocampal sclerosis is the most common type of drug-resistant epilepsy. Non-human primates are attractive models for studying the pathogenic mechanisms of TLE, with the goal of developing new drugs and interventions. In this study, we
Qun Wang et al.
Molecular neurobiology, 31(1-3), 3-16 (2005-06-15)
Neuronal excitation involving the excitatory glutamate receptors is recognized as an important underlying mechanism in neurodegenerative disorders. Excitation resulting from stimulation of the ionotropic glutamate receptors is known to cause the increase in intracellular calcium and trigger calcium-dependent pathways that
M Nakai et al.
Journal of neurochemistry, 74(2), 647-658 (2000-01-26)
The present study evaluated whether nuclear factor-kappaB (NF-kappaB) activation contributes to the apoptotic-like death of striatal neurons induced by kainic acid (KA) receptor stimulation. Intrastriatally infused KA (1.25-5.0 nmol) produced substantial neuronal loss as indicated by an 8-73% decrease in
Kyung-Ku Kang et al.
Laboratory animal research, 36, 39-39 (2020-11-03)
The kainic acid-induced seizure mouse model is widely used in epilepsy research. In this study, we applied kainic acid to the subcutaneous injections of three different sources of DBA/2 mice to compare and evaluate the seizure response. The three mouse
Zi-Qi Liu et al.
Toxicology, 435, 152408-152408 (2020-02-15)
To investigate the effects and mechanisms of NADPH on Kainic acid (KA)-induced excitotoxicity. KA, a non-N-methyl-d-aspartate glutamate receptor agonist, was exposed to adult SD rats via intrastriatal injection and rat primary cortical neurons to establish excitotoxic models in vivo and
N A Simonian et al.
Neuroscience, 75(4), 1047-1055 (1996-12-01)
Growing evidence suggests that non-N-methyl-D-aspartate receptor activation may contribute to neuronal death in both acute and chronic neurological diseases. The intracellular processes that mediate this form of neuronal death are poorly understood. We have previously characterized a model of kainic
Elizabeth A Pollina et al.
Nature, 614(7949), 732-741 (2023-02-16)
Neuronal activity is crucial for adaptive circuit remodelling but poses an inherent risk to the stability of the genome across the long lifespan of postmitotic neurons1-5. Whether neurons have acquired specialized genome protection mechanisms that enable them to withstand decades
Na Liu et al.
Redox biology, 73, 103176-103176 (2024-05-06)
Excitotoxicity is a prevalent pathological event in neurodegenerative diseases. The involvement of ferroptosis in the pathogenesis of excitotoxicity remains elusive. Transcriptome analysis has revealed that cytoplasmic reduced nicotinamide adenine dinucleotide phosphate (NADPH) levels are associated with susceptibility to ferroptosis-inducing compounds.
Lorena Ruiz-Clavijo et al.
Frontiers in neuroscience, 17, 1186256-1186256 (2023-07-27)
Hippocampal neurogenesis is a tightly regulated process in which neural stem cells (NSCs) get activated, enter in the cell cycle and give rise to neurons after a multistep process. Quiescent and activated NSCs, neural precursors, immature and mature neurons and
Vijay Swahari et al.
Cell reports, 35(1), 108946-108946 (2021-04-08)
Although embryonic brain development and neurodegeneration have received considerable attention, the events that govern postnatal brain maturation are less understood. Here, we identify the miR-29 family to be strikingly induced during the late stages of brain maturation. Brain maturation is
Brian J Wiltgen et al.
PloS one, 5(9), doi:10-doi:10 (2010-10-12)
A central concept in the field of learning and memory is that NMDARs are essential for synaptic plasticity and memory formation. Surprisingly then, multiple studies have found that behavioral experience can reduce or eliminate the contribution of these receptors to
Oksana Forostyak et al.
Stem cells and development, 22(10), 1506-1521 (2013-01-09)
Human embryonic stem cell-derived neural precursors (hESC NPs) are considered to be a promising tool for cell-based therapy in central nervous system injuries and neurodegenerative diseases. The Ca(2+) ion is an important intracellular messenger essential for the regulation of various
Hattie Chung et al.
Nature methods, 18(10), 1204-1212 (2021-10-06)
Identifying gene-regulatory targets of nuclear proteins in tissues is a challenge. Here we describe intranuclear cellular indexing of transcriptomes and epitopes (inCITE-seq), a scalable method that measures multiplexed intranuclear protein levels and the transcriptome in parallel across thousands of nuclei
Longze Sha et al.
JCI insight, 7(15) (2022-08-09)
Dysregulation of excitatory amino acid transporter 2 (EAAT2) contributes to the development of temporal lobe epilepsy (TLE). Several strategies for increasing total EAAT2 levels have been proposed. However, the mechanism underlying the oligomeric assembly of EAAT2, impairment of which inhibits
Brittany D Spitznagel et al.
Neurotoxicology, 95, 1-11 (2023-01-10)
Manganese (Mn) is an essential metal that serves as a cofactor for metalloenzymes important in moderating oxidative stress and the glutamate/glutamine cycle. Mn is typically obtained through the diet, but toxic overexposure can occur through other environmental or occupational exposure
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