[3H]MK-801 binding to forebrain of E1 (epileptic) and non-epileptic strains of mice

Kawasaki, Hiroaki; Itoh, Masatoshi; Nakahara, Tsutomu; Fukahori, Motofumi; Akazawa, Kouhei

doi:10.1016/0920-1211(91)90067-p

Cited by 5 publications

(2 citation statements)

References 14 publications

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“…Thcrefore, the switch of energy substrate in the brain from glucose to ketone bodies may affect synaptic activity in glutamatergic neurons. However, it is not likely that this is the mechanism of KD action because in our study learning behavior in KD-fed mice was not affected, and seizure susceptibility in EL has not previously bccn associated with an abnormality in the NMDA receptor complex (46). In KD-fed mice, the glucose consumption may not change, but the glucose oxidative metabolism may be decreased and compensated with ketone body oxidation.…”

Section: Influence Of the Kd On Associative Learningmentioning

confidence: 81%

The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy

et al. 2000

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Summary: Purpose: The ketogenic diet (KD) is a high-fat, low-carbohydratc and -protein diet that has been used to treat refractory seizures in children for more than 75 years. However, little is known about how the KD inhibits seizures or its el'fects on epilcptogcnesis. Several animal models of epilepsy have responded favorably to KD treatment, but the KD has not been studied in animals with a genetic predisposition to seizures. Here we studied the antiepileptogenic effect of the KD in EL mice, an animal model for human idiopathic epilepsy.M&ods: Young male EL mice (postnatal day 30) were randomly separated into two groups fed ad libitum with either the KD (treated, n = 21) or Agway chow (control, n = 19). The mice werc wcighcd and tested for seizures once per week for a total of 10 weeks. The effects of the KD on plasma levels of ketone bodies and glucose were analyzed at several time points throughout the study. Associative learning was compared between treated and control animals using a water maze.Results: KD treatment delayed seizure onset in young male EL mice by 1 month; however, seizure protection was transient, inasmuch as the treated and control mice experienced a similar number and intensity of seizures after 6 wccks on the diet. Plasma glucose levels and associativc learning were similar in the treated and control groups, but the plasma P-hydroxybutyrate levels were significantly highcr in mice on the KD. The level of ketosis, however, was not predictive of seizure protection in EL mice.Conclusion: The KD delayed seizure onset in EL mice, suggesting a transient protection against epileptogcnesis. The KD did not influence plasma glucose levels or learning. Therefore, the EL mousc may serve as a good model to study the antiepileptogenic mechanisms of the KD.

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Section: Influence Of the Kd On Associative Learningmentioning

confidence: 81%

The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy

et al. 2000

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“…The role of the NMDA receptor in EL mice is not yet clear (Oguro et al, 1990(Oguro et al, , 1991Kawasaki et al, 1991) . As aspartate is a potent NMDA receptor agonist (Patneau and Mayer, 1990;Pittaluga and Raiteri, 1992) and EL seizures can be blocked by NMDA receptor antagonists (Mori, 1988 ;Sato et al, 1990), it is possible that the NMDA receptor plays some role in EL seizures .…”

Section: Discussionmentioning

confidence: 99%

Enhanced Aspartate Release Related to Epilepsy in (EL) Mice

Flavin

Seyfried

1994

Journal of Neurochemistry

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Previous studies have shown that potassium‐evoked, calcium‐dependent, endogenous aspartate release is greater from hippocampal slices of adult epileptic (EL) mice than from nonepileptic control C57BL/6J (B6) mice. To examine further the association between epilepsy and enhanced aspartate release in EL mice, endogenous neurotransmitter release from hippocampal slices was studied in young, seizure‐free EL mice and in two nonseizure control mouse strains, DDY and B6. DDY is the parental strain from which EL arose, and it has a genetic background similar to EL. Released amino acid neurotransmitters were quantitated by HPLC with fluorescent detection and were expressed as picomoles of amino acid released per minute of incubation per slice ± SEM. Aspartate release was significantly higher in EL mice (15.8 ± 0.8) than in either the control B6 or DDY mice (8.5 ± 1.4 and 8.4 ± 1.7, respectively). No significant differences were found among the B6, DDY, and EL mice for the release of glutamate (23.0 ± 2.0, 32.3 ± 5.8, and 25.9 ± 2.6, respectively) or GABA (23.5 ± 0.7, 19.5 ± 3.2, and 21.8 ± 3.2, respectively). Thus, enhanced aspartate release precedes the onset of EL seizures and may be related to the cause rather than to the effects of seizure activity.

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Effects of MK-801, dantrolene, and FK506 on convulsive seizures and brain nitric oxide production in seizure-susceptible EL mice

et al. 2001

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[3H]MK-801 binding to forebrain of E1 (epileptic) and non-epileptic strains of mice

Cited by 5 publications

References 14 publications

The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy

The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy

Enhanced Aspartate Release Related to Epilepsy in (EL) Mice

Effects of MK-801, dantrolene, and FK506 on convulsive seizures and brain nitric oxide production in seizure-susceptible EL mice

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