Does antiepileptogenesis affects sleep in genetic epileptic rats?

Luijtelaar, Gilles van; Wilde, Matthias; Citraro, Rita; Scicchitano, Francesca; Rijn, Clementina M. van

doi:10.1016/j.ijpsycho.2011.09.010

Cited by 12 publications

(13 citation statements)

References 40 publications

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“…69,70 Even if basal cytokine levels are not substantially different between epileptic WAG/ Rij and non-epileptic control ACI rats, 71 after LPS challenge, an increase in absence epileptic activity in WAG/Rij rats is observed. 69,70 Even if basal cytokine levels are not substantially different between epileptic WAG/ Rij and non-epileptic control ACI rats, 71 after LPS challenge, an increase in absence epileptic activity in WAG/Rij rats is observed.…”

Section: Discussionmentioning

confidence: 99%

“…A strong link between absence seizures and inflammation in WAG/Rij rats has been shown. 69,70 Even if basal cytokine levels are not substantially different between epileptic WAG/ Rij and non-epileptic control ACI rats, 71 after LPS challenge, an increase in absence epileptic activity in WAG/Rij rats is observed. 70,72 Here, NaB counteracts the hepatic histopathological alterations, inflammation, and nitrosative stress related to chronic VPA treatment, highlighting its anti-inflammatory profile.…”

Section: Discussionmentioning

confidence: 99%

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Butyrate prevents valproate‐induced liver injury: In vitro and in vivo evidence

et al. 2019

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Sodium valproate (VPA), an antiepileptic drug, may cause dose-and time-dependent hepatotoxicity. However, its iatrogenic molecular mechanism and the rescue therapy are disregarded. Recently, it has been demonstrated that sodium butyrate (NaB) reduces hepatic steatosis, improving respiratory capacity and mitochondrial dysfunction in obese mice. Here, we investigated the protective effect of NaB in counteracting VPA-induced hepatotoxicity using in vitro and in vivo models. Human HepG2 cells and primary rat hepatocytes were exposed to high VPA concentration and treated with NaB. Mitochondrial function, lipid metabolism, and oxidative stress were evaluated, using Seahorse analyzer, spectrophotometric, and biochemical determinations.Liver protection by NaB was also evaluated in VPA-treated epileptic WAG/Rij rats, receiving NaB for 6 months. NaB prevented VPA toxicity, limiting cell oxidative and mitochondrial damage (ROS, malondialdehyde, SOD activity, mitochondrial bioenergetics), and restoring fatty acid oxidation (peroxisome proliferator-activated receptor α expression and carnitine palmitoyl-transferase activity) in HepG2 cells, primary hepatocytes, and isolated mitochondria. In vivo, NaB confirmed its activity normalizing hepatic biomarkers, fatty acid metabolism, and reducing inflammation and fibrosis induced by VPA. These data support the protective potential of NaB on VPA-induced liver injury, indicating it as valid therapeutic approach in counteracting this common side effect due to VPA chronic treatment. K E Y W O R D Santiepileptic drug, hepatotoxicity, lipid metabolism, mitochondrial dysfunction, oxidative stress, shortchain fatty acid | 677 PIROZZI et al. | 679 PIROZZI et al. incubated with tert-Butyl hydroperoxide (100 µM) plus H 2 O 2 for 3 hours. The fluorescence measurements were performed with aHTS-7000 Plus plate reader spectrofluorometer (Perkin Elmer, Wellesley, MA, USA) at 485 nm for excitation and 525 nm for emission wavelengths. ROS were quantified as percentage vs control unstimulated cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Butyrate prevents valproate‐induced liver injury: In vitro and in vivo evidence

et al. 2019

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“…This suggests that hypothalamic and brain stem structures known to be involved in REM sleep regulation, might also be affected by this chronic treatment (van Luijtelaar et al, 2012). …”

Section: Discussionmentioning

confidence: 99%

“…Also behavioral and sleep studies point towards the involvement of limbic and hypothalamic-brainstem changes in WAG/Rij rats accompanying epileptogenesis (van Luijtelaar, 2011; van Luijtelaar et al, 2012). Here the changes in depressive-like behavior pointing towards a role of the nucleus accumbens, part of the limbic circuitry, were counteracted by the early and chronic drug treatment.…”

Section: Discussionmentioning

confidence: 99%

Anti-epileptogenesis: Electrophysiology, diffusion tensor imaging and behavior in a genetic absence model

Luijtelaar¹,

Mishra²,

Edelbroek³

et al. 2013

Neurobiology of Disease

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The beneficial effects of chronic and early pharmacological treatment with ethosuximide on epileptogenesis were studied in a genetic absence epilepsy model comorbid for depression. It was also investigated whether there is a critical treatment period and treatment length. Cortical excitability in the form of electrical evoked potentials, but also to cortico-thalamo-cortical network activity (spike–wave discharges, SWD and afterdischarges), white matter changes representing extra corticothalamic functions and depressive-like behavior were investigated. WAG/Rij rats received either ethosuximide for 2 months (post natal months 2–3 or 4–5), or ethosuximide for 4 months (2–5) in their drinking water, while control rats drank plain water. EEG measurements were made during treatment, and 6 days and 2 months post treatment. Behavioral test were also done 6 days post treatment. DTI was performed ex vivo post treatment. SWD were suppressed during treatment, and 6 days and 2 months post treatment in the 4 month treated group, as well as the duration of AD elicited by cortical electrical stimulation 6 days post treatment. Increased fractional anisotropy in corpus callosum and internal capsula on DTI was found, an increased P8 evoked potential amplitude and a decreased immobility in the forced swim test. Shorter treatments with ETX had no large effects on any parameter. Chronic ETX has widespread effects not only within but also outside the circuitry in which SWD are initiated and generated, including preventing epileptogenesis and reducing depressive-like symptoms. The treatment of patients before symptom onset might prevent many of the adverse consequences of chronic epilepsy.

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“…Quantitative aspects are e.g. described by percentages total sleep, non-REM sleep, or REM sleep and by the number and duration of intermittent wakefulness periods, or sleep efficacy, for a study of the effects of the anti-absence drug ETX on sleep see van Luijtelaar et al (2012b). A major qualitative aspect of non-REM sleep is the amount of delta activity, by visual inspection of the sleep EEG it is difficult to establish the amount of specifically deep slow wave sleep.…”

Section: The Dependent Variablesmentioning

confidence: 99%

Establishing Drug Effects on Electrocorticographic Activity in a Genetic Absence Epilepsy Model: Advances and Pitfalls

Luijtelaar

Oijen

2020

Front. Pharmacol.

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The genetic rat models such as rats of the WAG/Rij strain and GAERS were developed as models for generalized genetic epilepsy and in particular for childhood absence epilepsy. These animal models were described in the eighties of the previous century and both models have, among others, face, construct and predictive validity. Both models were and are currently used as models to predict the action of antiepileptic medication and other experimental treatments, to elucidate neurobiological mechanisms of spike-wave discharges and epileptogenesis. Although the electroencephalagram (EEG)/ electrocorticogram (ECoG) is imperative for establishing absence seizures and to quantify the for absence epilepsy typical spike-wave discharges, monitoring the animals behavior is equally necessary. Here an overview is given regarding the design of drug evaluation studies, which animals to use, classical and new EEG variables, the monitoring and quantification of the behavior of the rats, some pitfalls regarding the interpretation of the data, and some developments in EEG technology.

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Does antiepileptogenesis affects sleep in genetic epileptic rats?

Cited by 12 publications

References 40 publications

Butyrate prevents valproate‐induced liver injury: In vitro and in vivo evidence

Butyrate prevents valproate‐induced liver injury: In vitro and in vivo evidence

Anti-epileptogenesis: Electrophysiology, diffusion tensor imaging and behavior in a genetic absence model

Establishing Drug Effects on Electrocorticographic Activity in a Genetic Absence Epilepsy Model: Advances and Pitfalls

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