Scopolamine-induced convulsions in food given fasted mice: effects of physostigmine and MK-801

Enginar, Nurhan; Nurten, Asiye; Yamantürk, Pınar; Koyuncuoğlu, H

doi:10.1016/s0920-1211(97)00041-7

Cited by 13 publications

(6 citation statements)

References 25 publications

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“…Animals deprived of food for 48 h were treated with 3 mg/kg, i.p., scopolamine or saline and were given food 20 min later. Scopolamine‐pretreated animals after starting to eat ad lib or a small amount in a restricted time (30 s) developed clonic convulsions in a few minutes, the incidence being 76% and 54%, respectively (Enginar et al., 1997). Demonstrating convulsions in 52‐h fasted rats afterward indicated that scopolamine‐induced seizures are not specific to mice (Nurten & Enginar, 2006).…”

Section: Scopolamine Induces Seizures In Fasted Mice and Rats After Fmentioning

confidence: 99%

“…Glutamate increases acetylcholine output in different brain regions through N ‐methyl‐ d ‐aspartate (NMDA) receptors (Ulus et al., 1992), and activation of α 2 ‐adrenergic receptors inhibits glutamate release (Kamisaki et al., 1991). Suppression of convulsions by the noncompetitive NMDA antagonist MK‐801 (Enginar et al., 1997) and α 2 ‐adrenergic agonists clonidine and tizanidine (Enginar et al., 1999) provides behavioral evidence, suggesting the involvement of glutamatergic hyperactivity in the seizures. Changes in [ 3 H]glutamate‐binding kinetics after 48 h of fasting imply adaptive responses in glutamatergic system during food deprivation as well (Enginar et al., 2003).…”

Section: Contribution Of Glutamatergic Activity To the Seizuresmentioning

confidence: 99%

“…A series of studies have shown that fasted mice and rats treated with antimuscarinics, scopolamine or atropine, develop seizures soon after being allowed to eat ad lib (Enginar et al, 1997(Enginar et al, , 1999(Enginar et al, , 2003(Enginar et al, , 2005Nurten & Enginar, 2006). Food deprivation itself, but not its hypoglycemic consequence, seems to be critical in the development of the seizures.…”

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Seizures triggered by food intake in antimuscarinic‐treated fasted animals: Evaluation of the experimental findings in terms of similarities to eating‐triggered epilepsy

Enginar¹,

Nurten²

2010

Epilepsia

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SUMMARYFood intake triggers convulsions in fasted mice and rats treated with antimuscarinic drugs, scopolamine or atropine. Bearing some similarities in triggering factor and manifestations of the seizures in patients with eating-evoked epilepsy, seizures in fasted animals may provide insight into the mechanism(s) of this rare and partially controlled form of reflex epilepsy. KEY WORDS: Antimuscarinic-induced seizures, Eating epilepsy, Fasting, Food deprivation, Food intake.A series of studies have shown that fasted mice and rats treated with antimuscarinics, scopolamine or atropine, develop seizures soon after being allowed to eat ad lib (Enginar et al

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Section: Scopolamine Induces Seizures In Fasted Mice and Rats After Fmentioning

confidence: 99%

Section: Contribution Of Glutamatergic Activity To the Seizuresmentioning

confidence: 99%

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confidence: 99%

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Seizures triggered by food intake in antimuscarinic‐treated fasted animals: Evaluation of the experimental findings in terms of similarities to eating‐triggered epilepsy

Enginar¹,

Nurten²

2010

Epilepsia

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“…Food deprivation for two days alters the [ 3 H]glutamate binding kinetics in the brain, which was antagonized by antimuscarinic treatment and food intake (Enginar et al, 2003). The other studies with antimuscarinic-induced convulsions showed that, many conventional and new antiepileptic drugs are ineffective in suppressing these convulsions (Enginar et al, 2005;Buget et al, 2016), whereas haloperidol, chlorpromazine, clonidine, tizanidine, and MK-801 were found to be effective (Enginar et al, 1997;.…”

Section: Introductionmentioning

confidence: 99%

Effects of scopolamine treatment and consequent convulsion development in c‑fos expression in fed, fasted, and refed mice

Türkmen

Nurten

Ergüven

et al. 2022

Acta Neurobiol. Exp.

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Fasting, anticholinergics, and seizures affect c-fos activation in the brain. Additionally, antimuscarinic treated fasted animals develop convulsion soon after re-feeding. Therefore, we assessed whether c-fos expression changes in fed, fasting, and refed animals and how scopolamine treatment affects these changes. We further assessed whether there is a change in c-fos expression after convulsions. For this purpose, BALB/c mice fasted for 1, 3, 6, 12, 24 and 48 h periods were used. The animals were treated with saline or scopolamine. Half of the animals treated with saline or scopolamine were given food 20 min after injection. All animals were observed for development of convulsions for 30 min. At the end of this period, the brains of all animals were removed, and the percentage of c-fos active cells in the hypothalamus was determined immunohistochemically. Convulsions occurred within 1-48 h of fasting, after scopolamine treatment and re-feeding. Compared to fed animals, c-fos expression was not significantly changed in those undergoing different fasting periods, but significantly decreased after 12 h fasting. After animals were allowed to eat, c-fos activation significantly increased in the 1, 3, 6 and 12 refed-saline groups and decreased in the 48 refed-saline group. Scopolamine treatment in 1-24 h fasted animals increased c-fos expression, but decreased in 48 h fasted animals. Whereas convulsion development in scopolamine-treated 3, 6, 12 and 24 h refed animals suppressed c-fos expression. These results demonstrate that re-feeding and scopolamine treatment induces neuronal activity in the hypothalamus, while scopolamine induced convulsions after food intake suppressed the c-fos activity.

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“…Then, we described that mice treated with scopolamine after fasting for 48 h have developed clonic convulsions soon after allowed to eat ad libitum. [1][2][3][4] The additive effect of scopolamine treatment and access to food is essential in the induction of convulsions. 5 Interestingly, scopolamine reverses convulsions elicited by the anticholinesterase compound Seizure (2006) Summary The present study was conducted to evaluate scopolamine-induced convulsions in fasted mice after food intake effects on the cortical electroencephalogram (EEG).…”

Section: Introductionmentioning

confidence: 99%

Electroencephalographic characterization of scopolamine-induced convulsions in fasted mice after food intake

Nurten

Özen

Karamürsel

et al. 2006

Seizure

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The present study was conducted to evaluate scopolamine-induced convulsions in fasted mice after food intake effects on the cortical electroencephalogram (EEG). Continuous EEG recordings were taken with Neuroscan for 10 min in freely moving mice with six chronic cortical electrode implants. Animals were weighed and deprived of food for 48 h. EEG recordings were taken at the 24th and 48th hour after their food deprivations. Later, all animals were treated with saline or scopolamine of 3mg/kg i.p. and EEG recordings were repeated for 10 min. Twenty minutes later, they were given food pellets and were allowed to eat ad libitum. All animals were observed for 60 min to determine the incidence and onset of convulsions and EEG recordings were taken simultaneously. The present results demonstrate that food deprivation causes differences in EEG in the elapsed time. The changes in EEG induced after food deprivation become different with scopolamine administration. In scopolamine treatment group, eating caused a series of high-voltage polyspikes and synchronized spikes with a predominant frequency in the 1-3 Hz range and fast activity that represents a typical epileptiform manifestation. It was concluded that the EEG properties and the behavioral patterns of these convulsions are in accordance with each other.

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Scopolamine-induced convulsions in food given fasted mice: effects of physostigmine and MK-801

Cited by 13 publications

References 25 publications

Seizures triggered by food intake in antimuscarinic‐treated fasted animals: Evaluation of the experimental findings in terms of similarities to eating‐triggered epilepsy

Seizures triggered by food intake in antimuscarinic‐treated fasted animals: Evaluation of the experimental findings in terms of similarities to eating‐triggered epilepsy

Effects of scopolamine treatment and consequent convulsion development in c‑fos expression in fed, fasted, and refed mice

Electroencephalographic characterization of scopolamine-induced convulsions in fasted mice after food intake

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