quinoline/seizures

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Pharmacological studies on 3-[gamma-(p-fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazino(1,2-a)quinoline hydrochloride (compound 69/183). Part IV: other CNS effects and acute toxicity.

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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

Adrenalectomy causes loss of zinc ions in zinc-enriched (ZEN) terminals and decreases seizure-induced neuronal death.

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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

Substituted hexahydrobenzo[f]thieno[c]quinolines as dopamine D1-selective agonists: synthesis and biological evaluation in vitro and in vivo.

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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.

Loss of zinc staining from hippocampal mossy fibers during kainic acid induced seizures: a histofluorescence study.

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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

Synthesis and anticonvulsant activity evaluation of 8-alkoxy-5-(4H-1,2,4-triazol-4-yl)quinoline derivatives.

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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,

Anticonvulsant and toxicity evaluation of some 7-alkoxy-4,5-dihydro-[1,2,4]triazolo[4,3-a]quinoline-1(2H)-ones.

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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,

Anticonvulsant activity and toxicity evaluation of Cu(II) and Zn(II) metal complexes derived from triazole-quinoline ligands.

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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

Design, synthesis and screening of quinoline-incorporated thiadiazole as a potential anticonvulsant.

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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

Some new 1-(2'-methyl-6'-methoxy-quinoline-4'-yl amino)-2-methyl-4-arylidene-imidazolin-5-ones as anticonvulsant and analgesic agents.

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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

Interactions of MRZ 2/576 with felbamate, lamotrigine, oxcarbazepine and topiramate in the mouse maximal electroshock-induced seizure model.

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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,

Modification of seizures elicited by the benzodiazepine Ro 5-3663--a comparison with picrotoxin.

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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

Evaluation of anticonvulsant activity of QUAN-0806 in various murine experimental seizure models.

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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 =

Design and synthesis of 5-alkoxy-[1,2,4]triazolo[4,3-a]quinoline derivatives with anticonvulsant activity.

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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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