Mirtazapine does not affect pentylenetetrazole- and maximal electroconvulsive shock-induced seizures in mice

Yılmaz, İsmail; Sezer, Zafer; Kayır, Hakan; Uzbay, Tayfun

doi:10.1016/j.yebeh.2007.04.004

Cited by 19 publications

(8 citation statements)

References 30 publications

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“…P18-P21 Scn1b +/− and Scn1b +/+ littermate mice were injected IP at doses between 0 and 80 mg/kg. Mice were observed for seizures in a large-sized cage that allowed exploration, with soft bedding, for 45 min, during which seizures were classified according to the Modified Racine scale (Racine, 1972; Cole et al, 2000; Witkin et al, 2007; Yilmaz et al, 2007). Following the experiment all animals were euthanized with an overdose of IP sodium pentobarbital (Ovation Pharmaceuticals, Deerfield, IL) followed by removal of vital organs.…”

Section: Methodsmentioning

confidence: 99%

A Functional Null Mutation ofSCN1Bin a Patient with Dravet Syndrome

et al. 2009

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Dravet syndrome (also called severe myoclonic epilepsy of infancy) is one of the most severe forms of childhood epilepsy. Most patients have heterozygous mutations in SCN1A, encoding voltage-gated sodium channel Na v 1.1 ␣ subunits. Sodium channels are modulated by ␤1 subunits, encoded by SCN1B, a gene also linked to epilepsy. Here we report the first patient with Dravet syndrome associated with a recessive mutation in SCN1B (p.R125C). Biochemical characterization of p.R125C in a heterologous system demonstrated little to no cell surface expression despite normal total cellular expression. This occurred regardless of coexpression of Na v 1.1 ␣ subunits. Because the patient was homozygous for the mutation, these data suggest a functional SCN1B null phenotype. To understand the consequences of the lack of ␤1 cell surface expression in vivo, hippocampal slice recordings were performed in Scn1b Ϫ/Ϫ versus Scn1b ϩ/ϩ mice. Scn1b Ϫ/Ϫ CA3 neurons fired evoked action potentials with a significantly higher peak voltage and significantly greater amplitude compared with wild type. However, in contrast to the Scn1a ϩ/Ϫ model of Dravet syndrome, we found no measurable differences in sodium current density in acutely dissociated CA3 hippocampal neurons. Whereas Scn1b Ϫ/Ϫ mice seize spontaneously, the seizure susceptibility of Scn1b ϩ/Ϫ mice was similar to wild type, suggesting that, like the parents of this patient, one functional SCN1B allele is sufficient for normal control of electrical excitability. We conclude that SCN1B p.R125C is an autosomal recessive cause of Dravet syndrome through functional gene inactivation.

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Section: Methodsmentioning

confidence: 99%

A Functional Null Mutation ofSCN1Bin a Patient with Dravet Syndrome

et al. 2009

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“…In experimental mice, myoclonic seizure (MCL), including twitches and straub tail reaction, clonic seizure (CL), tonic flexion (TF), and tonic extension (TE), were observed after PTZ administration (3 -5). Among these behaviors, MCL and CL observed in mice are mainly used as a model of human absence seizure in the field of behavioral pharmacology (6,7). On the other hand, the nucleus raphe magnus and the pontine reticular formation play an important role in the expression of MCL and CL, respectively (8,9).…”

Section: Introductionmentioning

confidence: 99%

Effects of Antiepileptics on Behavioral and Electroencephalographic Seizure Induced by Pentetrazol in Mice

et al. 2010

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Abstract. The present study was undertaken to investigate changes of the electroencephalogram (EEG) induced by pentetrazol (PTZ) in comparison with behavioral seizures in mice. Under pentobarbital anesthesia, mice were fixed to a stereotaxic apparatus, and electrodes were implanted into the frontal and occipital cortex. Behavioral and EEG changes were observed for 30 min following PTZ administration. After PTZ administration, mice showed myoclonic seizure (MCL) and clonic seizure (CL) in order. At the same time, spiking activity and spike-wave discharge in the cortex were observed. Phenobarbital, sodium valproate, diazepam, ethosuximide, and gabapentin caused a dose-dependent shortening of the duration of MCL and CL. In addition, they shortened the duration of spiking activity and spike-wave discharge dose-dependently. Moreover, phenytoin significantly inhibited the duration of spiking activity. It can be concluded that PTZinduced spiking activity and spike-wave discharge serve as useful indices to assess the potential of antiepileptic activity in absence and MCLs in humans. Moreover, it is supposed that employing an index of EEG activity in addition to that of behavioral activity is desirable for objectivity.

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“…The EMG recording was made and the AWR score was assessed in each session. The selection of 10 mg kg −1 was based on previous rodent/mouse studies 22,23 and the dose of 1 mg kg −1 was chosen to be close to that used in clinic.…”

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confidence: 99%