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quinoline/seizures

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3-[gamma-(p-Fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazino(1,2-a)quinoline hydrochloride (centpyraquin), a potent antihypertensive and tranquillising agent, was tested for anticonvulsant, analgesic and anti-inflammatory activities in mice and for anti-emetic activity in dogs. It did not
Chelatable zinc ions from synaptic vesicles have been suggested to be involved in neuronal death caused by stroke, epilepsy and head trauma. Elevated glucocorticoid concentration exacerbates such neuron loss, while low levels protect. We have tested the notion that the neuroprotective effect of
A series of substituted 9,10-dihydroxyhexahydrobenzo[f]thieno[c]quinolines (TB[f]Q), varying with respect to the position of the thiophene relative to the benzo[f]quinoline core and the nature and position of the substituent on the thiophene, were prepared and evaluated for their affinity and

Dopamine D1 receptor modulation of pilocarpine-induced convulsions.

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The contribution of dopaminergic mechanisms to the generalization of epileptic activity was studied in rats given pilocarpine after pretreatment with selective dopamine agonists. At the dose of 200 mg/kg, pilocarpine produced limbic stereotypes but not convulsions or seizure-related brain damage.
A quinoline fluorescence method for staining zinc in axonal boutons was used to study the effects of kainic acid (KA) induced seizures upon zinc in the boutons of hippocampal mossy fibers. Compared to untreated rats, rats given KA (10-12 mg/kg) and undergoing sustained seizures showed a marked loss
Two series of 8-alkoxy-5-(4H-1,2,4-triazol-4-yl)quinolines and 8-alkoxy-5-(2H-1,2,4-triazol-3-one-4-yl)quinolines were synthesized. The anticonvulsant activity of these compounds was evaluated with maximal electroshock seizure test and rotarod test. Among the synthesized compounds,
To further investigate anticonvulsant activity of quinoline derivatives, a series of 7-alkoxy-4,5-dihydro-[1,2,4]triazolo[4,3-a]quinoline-1(2H)-one derivatives was synthesized starting from 7-hydroxyl-3,4-dihydro-2(1H)-quinoline. In initial (phase I) screening and quantitative (phase II) evaluation,
A novel Cu(II) and Zn(II) complexes of triazolo-quinoline derivatives were synthesized by in situ method and were characterized by the spectro-analytical methods and their pharmacological properties were evaluated. The compound C3 has exhibited promising anticonvulsant activity towards the
A series of quinoline-incorporated substituted thiadiazole were designed and synthesized using appropriate synthetic route keeping in view the structural requirement of pharmacophore and evaluated for anticonvulsant and CNS activities. After intraperitoneal injection to mice, some synthesized
Seventeen new 1-(2'-methyl-6'-methoxyquinoline-4'-yl-amino)-2-methyl-4-arylideneimidazol-5-ones have been synthesized by the condensation between the respective azlactones (prepared by the well known Erlenmeyer azlactone synthesis) and 2-methyl-4 hydrazino-6-methoxy-quinolines. The compounds have
This study focused on the evaluation of interactions between MRZ 2/576 (8-chloro-4-hydroxy-1-oxo-1,2-dihydropyridazino(4,5-b)quinoline-5-oxide choline salt), an N-methyl-D-aspartate (NMDA) receptor antagonist acting at the NMDA receptor/glycine(B) site and four newer antiepileptic drugs (felbamate,
Ro 5-3663 is a convulsant 1,4-benzodiazepine that does not act at the benzodiazepine, but at the picrotoxin, site. To characterize the behavioural actions of Ro 5-3663, a comparison was made between its effects and those of picrotoxin, when combined with several compounds that act at the
A new quinoline derivative, QUAN-0806 (7-hexyloxy-5-phenyl-1,2,4-triazolo[4,3-alpha]quinoline) was tested for anticonvulsant activity using the maximal electroshock seizure (MES) and the rotarod neurotoxicity (Tox) tests in mice. The MES test showed that QUAN-0806 exhibited higher activity (ED50 =
A series of 5-alkoxy-[1,2,4]triazolo[4,3-a]quinoline derivatives were synthesized using 4-hydroxyquinolin-2(1H)-one as the starting material. Their anticonvulsant activities were evaluated by the maximal electroshock test (MES) and their neurotoxicities were measured by the rotarod test. The results

Translocation of zinc may contribute to seizure-induced death of neurons.

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Rats were subjected to seizures induced by kainic acid, and the resulting changes in CNS zinc staining were studied with the toluene sulfonamide quinoline fluorescence method. Seizures caused a loss of zinc staining from presynaptic boutons in many limbic and cerebrocortical regions. Simultaneously,
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