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staurosporine/seizures
Veza se sprema u međuspremnik
Stranica 1 iz 20 rezultatima
Excitatory amino acid-elicited tonic convulsions in mice and N-methyl-D-aspartate receptor activation: role of Ca(2+) influx and involvement of intracellular Ca(2+)-dependent biochemical processes.
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Intravenously administered nimodipine (an L-type Ca(2+) antagonist) as well as dizocilpine (an N-methyl-D-aspartate--NMDA--antagonist) showed a wide spectrum of anticonvulsant activity in intracerebroventricular mouse models for excessive activation of excitatory amino acid receptors. The duration
Transgenic mice neuronally expressing baculoviral p35 are resistant to diverse types of induced apoptosis, including seizure-associated neurodegeneration.
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Apoptosis is a cell-suicide process that appears to play a central role not only during normal neuronal development but also in several neuropathological disease states. An important component of this process is a proteolytic cascade involving a family of cysteine proteases called caspases. Caspase
Bacterial alkaloids mitigate seizure-induced hippocampal damage and spatial memory deficits.
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Studies of human patients with temporal lobe epilepsy and animal models of epilepsy have established relationships between seizures, excitotoxic hippocampal damage, and memory impairment. We report that bacterial alkaloids, recently shown to mimic actions of neurotrophic factors in cell culture,
Expression of seizure-related PTZ-17 is induced by potassium deprivation in cerebellar granule cells.
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The aim of this study was to identify changes in gene expression during neuronal apoptosis using the differential display (DD) technique. Potassium deprivation was used to induce neuronal apoptosis in cultured rat cerebellar granule cells. DD analysis of about 1600 transcripts resulted in 8 cDNA
Bok Is Not Pro-Apoptotic But Suppresses Poly ADP-Ribose Polymerase-Dependent Cell Death Pathways and Protects against Excitotoxic and Seizure-Induced Neuronal Injury.
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Bok (Bcl-2-related ovarian killer) is a Bcl-2 family member that, because of its predicted structural homology to Bax and Bak, has been proposed to be a pro-apoptotic protein. In this study, we demonstrate that Bok is highly expressed in neurons of the mouse brain but that bok was not required for
Potassium channel gene therapy can prevent neuron death resulting from necrotic and apoptotic insults.
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Necrotic insults such as seizure are excitotoxic. Logically, membrane hyperpolarization by increasing outwardly conducting potassium channel currents should attenuate hyperexcitation and enhance neuron survival. Therefore, we overexpressed a small-conductance calcium-activated (SK2) or voltage-gated
Caffeine-induced inhibition of the activity of glutamate transporter type 3 expressed in Xenopus oocytes.
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Caffeine has been known to trigger seizures, however, the precise mechanism about the proconvulsive effect of caffeine remains unclear. Glutamate transporters play an important role to maintain the homeostasis of glutamate concentration in the brain tissue. Especially, dysfunction of excitatory
17β-Estradiol attenuates the activity of the glutamate transporter type 3 expressed in Xenopus oocytes.
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Estrogen, a neuroactive sex hormone in the brain, enhances neuronal excitability and increases seizures. Glutamate transporters help in limiting the excitatory neurotransmission by uptaking glutamate from the synapses. We investigated the effects of 17β-estradiol on the activity of a glutamate
Nicotine decreases the activity of glutamate transporter type 3.
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Nicotine, the main ingredient of tobacco, elicits seizures in animal models and cigarette smoking is regarded as a behavioral risk factor associated with epilepsy or seizures. In the hippocampus, the origin of nicotine-induced seizures, most glutamate uptake could be performed primarily by
Influence of hypotonic shock on glutamate and GABA uptake in rat brain synaptosomes.
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Hyponatremia leads to hyperexcitability of neurons, seizures, and coma. It is well established that uptake of neurotransmitters is a sodium-dependent process. Therefore, we suggest that inhibition of neurotransmitter uptake can lead to the clinical manifestations of hyponatremia. Decreasing of
Potentiation of tonic GABAergic inhibition by activation of postsynaptic kainate receptors.
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Presynaptic kainate-type glutamate ionotropic receptors (KARs) that mediate either the depression or the facilitation of GABA release have been intensively studied. Little attention has been given to the modulation of GABAA receptors (GABAARs) by postsynaptic KARs. Recent studies suggest that two
Expression and subcellular localization of thymosin beta15 following kainic acid treatment in rat brain.
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Thymosin beta15 (Tbeta15) is a pleiotropic factor which exerts multiple roles in the development of nervous system and brain diseases. In this study, we found that the expressions of Tbeta15 mRNA and protein were substantially increased in several brain regions including hippocampal formation and
The protein kinase C activators, phorbol 12-myristate,13-acetate and phorbol 12,13-dibutyrate, are convulsant in the pico-nanomolar range in mice.
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Administration of phorbol 12-myristate,13-acetate (PMA, 10 fmol-10 nmol) or phorbol 12,13-dibutyrate (PDB, 0.2-495 nmol) (i.c.v.) to mice induced: hindlimb scratching, tremor, myoclonic jerks, hyperlocomotion, clonic seizure, followed by death or recovery. CD50 values for clonic seizures for PMA and
CLN3 defines a novel antiapoptotic pathway operative in neurodegeneration and mediated by ceramide.
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Juvenile neuronal ceroid lipofuscinosis or Batten disease (JNCL) is a neurodegenerative disorder characterized by blindness, seizures, cognitive decline and early death. Brain atrophy and retinitis pigmentosa ensue because of neuronal and photoreceptor apoptosis. The CLN3 gene defective in JNCL
Induction of Per1 expression following an experimentally induced epilepsy in the mouse hippocampus.
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The Period1 (Per1) is a clock-oscillating gene product that plays an essential role in the generation and modulation of circadian rhythm in the suprachiasmatic nucleus (SCN) of hypothalamus. However, Per1 is also expressed in many other brain regions including cerebral cortex, hippocampus, and
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