nicotine/epileptische aanval

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Tobacco smoking, epilepsy, and seizures.

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Tobacco smoking is considered the greatest risk factor for death caused by noncommunicable diseases. In contrast to extensive research on the association between tobacco smoking and diseases such as heart attack, stroke, and cancers, studies on the association between tobacco smoking and seizures or

Mediation of nicotine-induced convulsions by central nicotinic receptors of the 'C6' type.

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The nature of the central receptors mediating the convulsant actions of nicotine has been investigated. Clonic tonic convulsions were seen in mice following intracerebroventricular (i.c.v.) injection of nicotinic agonists. (-)Nicotine was the most potent agonist tested, with a CD50 of 7.9 X 10(-9)

Ethanol blocks nicotine-induced seizures in mice: comparison with midazolam and baclofen.

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Low doses of ethanol may antagonize the pharmacological effects of nicotine. Recently, it has been shown that the effects of ethanol on nicotine discrimination are not correlated with blood ethanol levels. The aim of the present study was to evaluate whether ethanol (0.5-2g/kg, i.p.) could block

The intrahippocampal administration of the neurosteroid allopregnanolone blocks the audiogenic seizures induced by nicotine.

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Allopregnanolone (AlloP), GABA(A) positive modulator, has efficacy as anticonvulsant. In contrast, nicotine and pregnenolone sulfate (PregS) act as potent convulsants. The present study aims to evaluate whether a promnesic dose of PregS and/or an anxiolytic dose of AlloP administered in the

Protective effect of α-asarone against nicotine-induced seizures in mice, but not by its interaction with nicotinic acetylcholine receptors.

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Alpha-asarone is one of the bioactive phytochemicals present in the rhizomes of Acorus species and demonstrated its anticonvulsant activity in rodents. Alpha-asarone protected mice from the gamma-aminobutyric acid (GABA) type A receptor antagonist or N-methyl-d-aspartate (NMDA) receptor

Peripheral and central routes of administration of quaternary ammonium compound IEM-1460 are equally potent in reducing the severity of nicotine-induced seizures in mice.

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Peripheral administration of nicotinic receptor antagonists with a quaternary ammonium group (hexamethonium and chlorisondamine) did not prevent the development of seizures induced by systemic treatment with nicotine in the toxic dose. The Me3N+ group with stable positive charge inhibits transport

Different effects of nitric oxide synthase inhibitors on convulsions induced by nicotine in mice.

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Acute intraperitoneal (i.p.) administration of N(G)-nitro-L-arginine (NNA, 10, 20 and 40 mg/kg), a non-selective nitric oxide synthase (NOS) inhibitor, significantly and dose-dependently decreased the incidence of convulsions induced by i.p. nicotine (NIC) in mice, whereas 7-nitroindazole (7NI, 50

Adverse Experience Reports of Seizures in Youth and Young Adult Electronic Nicotine Delivery Systems Users.

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Electronic nicotine delivery systems (ENDS) use poses significant and avoidable health risks to young people. Until recently, seizures were most often associated with cases of liquid nicotine ingestion.We examined 122 voluntary reports of seizures (n = 114)

Nicotine increases eclampsia-like seizure threshold and attenuates microglial activity in rat hippocampus through the α7 nicotinic acetylcholine receptor.

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A considerable number of studies have demonstrated that nicotine, a α7-nicotinic acetylcholine receptor (α7-nAChR) agonist, can dampen immune response through the cholinergic anti-inflammatory pathway. Evidence suggests that inflammation plays a critical role in eclampsia, which contributes to

Mice lacking neuronal nicotinic acetylcholine receptor beta4-subunit and mice lacking both alpha5- and beta4-subunits are highly resistant to nicotine-induced seizures.

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Nicotine, the main addictive component of tobacco, evokes a wide range of dose-dependent behaviors in rodents, and when administrated in high doses, it can induce clonic-tonic seizures. Nicotine acts through the nicotinic acetylcholine receptors (nAChRs). Mutations in the human alpha4- and the

Sensitivity to the seizure-inducing effects of nicotine is associated with strain-specific variants of the alpha 5 and alpha 7 nicotinic receptor subunit genes.

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Restriction fragment length polymorphisms (rflps) have been identified for the nicotinic ACh receptor subunit genes alpha 5 and alpha 7 between two mouse strains (C3H/2ibg and DBA/2ibg) that differ in sensitivity to the convulsant effects of nicotine. In the study reported here, F2 animals derived

The alpha3 and beta4 nicotinic acetylcholine receptor subunits are necessary for nicotine-induced seizures and hypolocomotion in mice.

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Binding of nicotine to nicotinic acetylcholine receptors (nAChRs) elicits a series of dose-dependent behaviors that go from altered exploration, sedation, and tremors, to seizures and death. nAChRs are pentameric ion channels usually composed of alpha and beta subunits. A gene cluster comprises the

Increased sensitivity to nicotine-induced seizures in mice heterozygous for the L250T mutation in the alpha7 nicotinic acetylcholine receptor.

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alpha7 Nicotinic acetylcholine receptors (nAChRs) are sparsely distributed throughout the peripheral and central nervous systems. Several studies have suggested that central alpha7 nicotinic receptors may influence sensitivity to nicotine-induced seizures in mice. In order to investigate the effect

Chronic nicotine pretreatment protects the blood-brain barrier against nicotine-induced seizures in the rat.

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This study was designed to investigate the possible protective actions of nicotine on cerebrovascular permeability in convulsions during nicotine-induced seizures. We have measured the permeability changes in the blood-brain barrier (BBB) macroscopically and spectrophotometrically by using Evans

Maturational changes related to dopamine in the effects of d-amphetamine, cocaine, nicotine, and strychnine on seizure susceptibility.

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The effects of four neural excitants (damphetamine, cocaine, nicotine, and strychnine) on myoclonic and clonic seizure susceptibility were investigated in two age groups (30 and 120 days) of short-sleep mice. Amphetamine and cocaine decreased susceptibility to myoclonus in young mice and increased

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