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Showing 1-30 of 85 results for "K0250" within Papers
CA3 Synaptic Silencing Attenuates Kainic Acid-Induced Seizures and Hippocampal Network Oscillations.
Lily M Y Yu et al.
eNeuro, 3(1) (2016-03-30)
Epilepsy is a neurological disorder defined by the presence of seizure activity, manifest both behaviorally and as abnormal activity in neuronal networks. An established model to study the disorder in rodents is the systemic injection of kainic acid, an excitatory
Ursula S Sandau et al.
Epilepsia, 60(4), 615-625 (2019-03-01)
Over one-third of all patients with epilepsy are refractory to treatment and there is an urgent need to develop new drugs that can prevent the development and progression of epilepsy. Epileptogenesis is characterized by distinct histopathologic and biochemical changes, which
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
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
J T Coyle
Ciba Foundation symposium, 126, 186-203 (1987-01-01)
Kainic acid, an acidic pyrolidine isolated from the seaweed Digenea simplex, is the most potent of the commonly used exogenous excitotoxins. The neurotoxic threshold of kainic acid is nearly two magnitudes lower than that of the other receptor-specific agonists, N-methyl-D-aspartic
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
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
Karina Hernández Mercado et al.
Neural plasticity, 2022, 7432842-7432842 (2022-10-11)
The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG
A Skliris et al.
Cell death and differentiation, 22(5), 703-718 (2014-10-11)
Alterations in the functions of neuronal RNA-binding proteins (RBPs) can contribute to neurodegenerative diseases. However, neurons also express a set of widely distributed RBPs that may have developed specialized functions. Here, we show that the ubiquitous member of the otherwise
Natural products regulate mitochondrial function in cognitive dysfunction-A scoping review.
Tuo, et al.
Frontiers in Pharmacology, 14, 1091879-1091879 (2023)
Jia-Hua Hu et al.
Nature communications, 11(1), 1567-1567 (2020-03-29)
Voltage-gated K+ channels function in macromolecular complexes with accessory subunits to regulate brain function. Here, we describe a peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1)-dependent mechanism that regulates the association of the A-type K+ channel subunit Kv4.2 with its auxiliary subunit
Fudong Liu et al.
Stroke, 40(5), 1842-1848 (2009-03-07)
Over the past 5 years, experimental data have emerged that ischemia-induced cell death pathways may differ in males and females. Cell death in males is triggered by poly(ADP-ribose) polymerase activation and nuclear translocation of apoptosis-inducing factor. We have previously shown
Qin Yang et al.
EBioMedicine, 47, 470-483 (2019-09-03)
NACHT and WD repeat domain-containing protein 1 (Nwd1) is a member of the innate immune protein subfamily. Nwd1 contributes to the androgen receptor signaling pathway and is involved in axonal growth. However, the mechanisms that underlie pathophysiological dysfunction in seizures
Qays Kharouf et al.
British journal of pharmacology, 177(16), 3712-3729 (2020-05-05)
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are encoded by four genes (HCN1-4) with distinct biophysical properties and functions within the brain. HCN4 channels activate slowly at robust hyperpolarizing potentials, making them more likely to be engaged during hyperexcitable neuronal network activity
Seiichiro Jinde et al.
The European journal of neuroscience, 30(6), 1036-1055 (2009-09-09)
Gamma oscillations are a prominent feature of hippocampal network activity, but their functional role remains debated, ranging from mere epiphenomena to being crucial for information processing. Similarly, persistent gamma oscillations sometimes appear prior to epileptic discharges in patients with mesial
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
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
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
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
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
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
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
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
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)
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
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