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l glutamic acid/епилептични припадъци
Линкът е запазен в клипборда
Страница 1 от 30 резултата
Seizures and the dose of L-glutamic acid in rats.
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[ON INDUCTION OF CONVULSIONS AFTER INTRATHECAL INJECTION OF L-GLUTAMIC ACID].
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Simultaneous glutamate and EEG activity measurements during seizures in rat hippocampal region with the use of an electrochemical biosensor.
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Excessive release of L-glutamic acid (glu) has been associated with seizures and epilepsy. Some microdialysis studies have demonstrated an increase in glu levels during seizures both in human and in different animal models of experimental epilepsy. With these techniques it is difficult to monitor
GABA and L-glutamic acid release in en bloc resection slices of human hippocampus: an in vitro microdialysis study.
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The interaction of neurotransmitters has been a major interest in pathophysiological conditions like epilepsy. In vivo microdialysis has recently gained much validity in measuring neurotransmitter release in experimental animals. However, there is a paucity of data concerning its use in humans on
Comparison of neurotropic effects of L-glutamic acid and its new derivative β-phenylglutamic acid hydrochloride (RGPU-135, glutarone).
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In contrast to L-glutamic acid (200 mg/kg), β-phenylglutamic acid hydrochloride (26 mg/kg) produces no anticonvulsant effects during generalized convulsions induced by "maximum electric shock". However, β-phenylglutamic acid hydrochloride was more potent than L-glutamic acid in increasing survival
A dipeptide derived from kainic and L-glutamic acids: a selective antagonist of amino acid induced neuroexcitation with anticonvulsant properties.
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The dipeptide N-[[[2'S-(2' alpha, 3' beta, 4' beta)]-2'-carboxy-4'-(1"-methylethenyl)-3'-pyrrolidinyl)acetyl]-L- glutamic acid (6) has been synthesized by a route that involves the selective protection of the alpha-carboxyl function of kainic acid. This dipeptide inhibits the stimulation of Na+
Exogenous protein Hsp70/Hsc70 can penetrate into brain structures and attenuate the severity of chemically-induced seizures.
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Heat shock protein 70 kDa (Hsp70) possesses a remarkable neuroprotective activity and the results of recent studies demonstrated its efficacy in the attenuation of epileptic seizures. The aim of this study was to explore the effects of a pure Hsp70/Hsc70 preparation delivered to the brain regions
Effects of anticonvulsants and other agents on seizures induced by intracerebral L-glutamate.
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Convulsions induced in mice by intracerebral injection of L-glutamate were antagonized by phenytoin, phenobarbital, chlordiazepoxide and valproic acid. Trimethadione had only a small effect at the dose used, and ethosuximide was ineffective. The profile of interaction of glutamate with these
NMDA and not non-NMDA receptor antagonists are protective against seizures induced by homocysteine in neonatal rats.
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Homocysteine induces seizures in adult, as well as in immature, experimental animals, but the mechanism of its action is still unknown. The aim of the present study was to examine whether homocysteine in immature animals may act via excitatory amino acids receptors. Seizures were induced in
Some correlations between local anesthetic-induced convulsions and gamma-aminobutyric acid in rat spinal cord.
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The effects of local anesthetics (procaine and lidocaine) on the gamma-aminobutyric acid (GABA) and L-glutamic acid (Glu) levels in rat spinal cord were studied during the convulsive process. The present study also investigated the influence of central GABA manipulations on the local
Extracellular hypothalamic gamma-aminobutyric acid (GABA) and L-glutamic acid concentrations in response to bicuculline in a genetic absence epilepsy rat model.
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The posterior part of the hypothalamus plays a vital role in the homeostatic processes of the internal environment, including blood pressure and heart rate regulation, by means of gamma-aminobutyric acid (GABA)ergic and glutamatergic neurotransmission. In this study we measured the extracellular
Blockade of hyperbaric oxygen induced seizures by excitatory amino acid antagonists.
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The effectiveness of several excitatory amino acid antagonists to delay or block seizures induced by oxygen at high pressure was examined in mice. Of the antagonists tested, namely, L-proline, DL-alpha-aminoadipate, DL-2-amino-5-phosphonovalerate, and L-glutamic acid diethyl ester,
Susceptibility to seizures produced by pilocarpine in rats after microinjection of isoniazid or gamma-vinyl-GABA into the substantia nigra.
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Pilocarpine, given intraperitoneally to rats, reproduces the neuropathological sequelae of temporal lobe epilepsy and provides a relevant animal model for studying mechanisms of buildup of convulsive activity and pathways operative in the generalization and propagation of seizures within the
Spinal seizures evoked by sudden cooling of amphibian isolated spinal cords: involvement of excitatory amino acids.
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Sudden cooling of the isolated spinal cord of frogs results in characteristic seizure-like activity in the hind legs. In the present investigation, these spinal seizures induced by sudden cooling (SSSC) were studied to determine whether excitatory amino acids (EAAs) are involved in the mediation of
NNZ-2566, a glypromate analog, attenuates brain ischemia-induced non-convulsive seizures in rats.
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Ischemic and traumatic brain injuries often induce non-convulsive seizures (NCSs), which likely contribute to the worsening of neurological outcomes. Here, we evaluated the effect of glycyl-L-methylprolyl-L-glutamic acid (NNZ-2566) to lessen the severity of NCSs caused by permanent middle cerebral
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