rotenone/seizures

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Oxidative storm in a patient with acute rotenone-containing plant poisoning.

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A 64-year-old woman presented with coma, seizure, and lactic acidosis after ingesting 80 yam bean seeds. This rotenone-containing seeds cause cellular asphyxia via blockage of the mitochondrial electron transport. Subsequent oxidative stress results in the formation of lipid peroxidation (LPO).

Seizure activity and cortical spreading depression monitored by an extrinsic potential-sensitive molecular probe.

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Using surface fluorescence and reflectance measurements from the exposed cerebral cortex, several potential-sensitive molecular probes, primarily oxonol V, have been evaluated as indicators of electrical activity changes developing during seizure activity in the mongolian gerbil. Intraventricular

Targeting deficiencies in mitochondrial respiratory complex I and functional uncoupling exerts anti-seizure effects in a genetic model of temporal lobe epilepsy and in a model of acute temporal lobe seizures.

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Mitochondria actively participate in neurotransmission by providing energy (ATP) and maintaining normative concentrations of reactive oxygen species (ROS) in both presynaptic and postsynaptic elements. In human and animal epilepsies, ATP-producing respiratory rates driven by mitochondrial

The role of astrocytes in seizure generation: insights from a novel in vitro seizure model based on mitochondrial dysfunction.

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Approximately one-quarter of patients with mitochondrial disease experience epilepsy. Their epilepsy is often severe and resistant towards conventional antiepileptic drugs. Despite the severity of this epilepsy, there are currently no animal models available to provide a mechanistic understanding of

NMDA-induced superoxide production and neurotoxicity in cultured rat hippocampal neurons: role of mitochondria.

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Excitotoxic mechanisms are believed to be involved in the death of neurons after trauma, epileptic seizures and cerebral ischaemia. We investigated the role of mitochondrial superoxide production in excitotoxic cell death of cultured rat hippocampal neurons. Brief exposure to the selective glutamate

A Metabolic Mechanism for Anaesthetic Suppression of Cortical Synaptic Function in Mouse Brain Slices-A Pilot Investigation

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Regulation of synaptically located ionotropic receptors is thought to be the main mechanism by which anaesthetics cause unconsciousness. An alternative explanation, which has received much less attention, is that of primary anaesthetic disruption of brain metabolism via suppression of mitochondrial

Opposing effects of 2-deoxy-d-glucose on interictal- and ictal-like activity when K+ currents and GABAA receptors are blocked in rat hippocampus in vitro.

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The ketogenic diet (KD), a high-fat, carbohydrate-restricted diet, is used as an alternative treatment for drug-resistant epileptic patients. Evidence suggests that compromised glucose metabolism has a significant role in the anticonvulsant action of the KD; however, it is unclear what part of the

Infant-onset progressive myoclonus epilepsy.

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We report the clinical, electroencephalographic, neurophysiologic, and neuroimaging findings in eight children with infant-onset progressive myoclonus epilepsy, all of whom had muscle biopsies performed as as part of the diagnostic evaluation. Each child had myoclonic seizures, generalized

A mitochondrial encephalomyopathy with cardiomyopathy. A case revealing a defect of complex I in the respiratory chain.

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We describe a 16-year-old Japanese girl with a mitochondrial encephalomyopathy who presented with progressive dementia, limb weakness and atrophy, episodic vomiting, generalized convulsions, myoclonic seizures, and hypertrophic cardiomyopathy. CT scan revealed transient focal low density areas in

Sulforaphane is anticonvulsant and improves mitochondrial function.

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The nuclear factor erythroid 2-related factor 2 pathway (Nrf2) has been previously identified to protect the brain against various impacts. Here, we investigated the effect of the Nrf2 activator sulforaphane in various seizure models and hippocampal mitochondrial bioenergetics. We found that daily

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