Learning and memory impairment in rats with chronic atypical absence seizures

Chan, Kin; Jia, Zhengping; Murphy, Patricia A.; Burnham, W. McIntyre; Cortez, Miguel A.; Snead, O. Carter

doi:10.1016/j.expneurol.2004.08.001

Cited by 50 publications

(42 citation statements)

References 57 publications

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“…Dissociation between epileptiform discharges and cognitive dysfunction was also shown in a rat model of atypical absence seizures, the AY-9944 model (Chan et al 2004; Cortez et al 2001). Repetitive administration of AY-9944, a cholesterol biosynthesis inhibitor, in PN2, PN8, PN14, PN20 Long Evans hooded rats results in persisting appearance of recurrent, spontaneous atypical bursts of 4-6Hz slow spike wave discharges (SSWDs) (Cortez et al 2001) and show impairment in spatial learning and working memory in the radial arm maze test (Chan et al 2004).…”

Section: Models Studying the Impact Of Subclinical Epileptiform DImentioning

confidence: 81%

Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies

Galanopoulou

Moshé

2015

Neurobiology of Disease

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Early onset and infantile epileptic encephalopathies (EIEEs) are usually associated with medically intractable or difficult to treat epileptic seizures and prominent cognitive, neurodevelopmental and behavioral consequences. EIEEs have numerous etiologies that contribute to the inter- and intra-syndromic phenotypic variability. Etiologies include structural and metabolic or genetic etiologies although a significant percentage is of unknown cause. The need to better understand their pathogenic mechanisms and identify better therapies has driven the development of animal models of EIEEs. Several rodent models of infantile spasms have emerged that recapitulate various aspects of the disease. The acute models manifest epileptic spasms after induction and include the NMDA rat model, the NMDA model with prior prenatal betamethasone or perinatal stress exposure, and the γ-butyrolactone induced spasms in a mouse model of Down syndrome. The chronic models include the tetrodotoxin rat model, the aristaless related homeobox X-linked (Arx) mouse models and the multiple-hit rat model of infantile spasms. We will discuss the main features and findings from these models on target mechanisms and emerging therapies. Genetic models have also provided interesting data on the pathogenesis of Dravet syndrome and proposed new therapies for testing. The genetic associations of many of the EIEEs have also been tested in rodent models as to their pathogenicity. Finally, several models have tested the impact of subclinical epileptiform discharges on brain function. The impact of these advances in animal modeling for therapy development will be discussed.

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Section: Models Studying the Impact Of Subclinical Epileptiform DImentioning

confidence: 81%

Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies

Galanopoulou

Moshé

2015

Neurobiology of Disease

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“…Atypical seizures are characterized by drug resistance and are usually associated with symptomatic epilepsies and epileptic encephalopathies [19,36]. Additionally, unlike typical absence seizures, these seizures show clear evidence of hippocampal and temporal lobe circuitry involvement [17,18,37]. A study with a genetic mouse model of atypical absence seizures showed that GSWDs arose from the midline thalamus and hippocampus [37].…”

Section: Initial-response Group (N = 12)mentioning

confidence: 97%

“…Atypical absence seizures, on the other hand, are invariably associated with severe symptomatic or cryptogenic epilepsies, and tend to be refractory to AED medication [19]. Based on the clear association of both temporal lobe involvement and drug refractoriness with a typical absence seizures [17,18], we hypothesize that temporal involvement in seizure generation may be an indicator of drug refractoriness.…”

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confidence: 98%

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Temporal current-source of spikes suggests initial treatment failure in childhood absence epilepsy

Yeom

Kim

Lee

et al. 2015

Seizure

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“…In this model, AY-9944 is given to rat pups. AY-9944 inhibits the reduction of 7-dehydrocholesterol to cholesterol [97][98][99][100]. For reasons that are not entirely clear, the rats begin having atypical absences during preadolescence [98].…”

Section: Absence Seizuresmentioning

confidence: 99%

Choosing the Correct Antiepileptic Drugs: From Animal Studies to the Clinic

Holmes¹,

Zhao²

2008

Pediatric Neurology

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Epilepsy is a chronic condition caused by an imbalance of normal excitatory and inhibitory forces in the brain. Antiepileptic drug therapy has been directed primarily toward reducing excitability through blockage of voltage-gated Na + or Ca 2+ channels, or increasing inhibition through enhancement of γ-aminobutyric acid currents. Prior to clinical studies, putative antiepileptic drugs are screened in animals, usually rodents. Maximal electrical shock, pentylenetetrazol, and kindling are typically used as non-mechanistic screens for antiseizure properties and the rotorod test for assessing acute toxicity. While antiseizure drug screening has been successful in bringing drugs to the market and improving our understanding of the pathophysiology of seizures, it should be emphasized that the vast majority of drug screening occurs in mature male rodents and involves models of seizures, not epilepsy. Effective drugs in acute seizures may not be effective in chronic models of epilepsy. Seizure type, clinical and electroencephalographic phenotype, syndrome, and etiology are often quite different in children with epilepsy than adults. Despite these age-related unique features, drugs used in children are generally the same as used in adults. As awareness of the unique features of seizures during development increases, it is anticipated that more drug screening in the immature animal will occur.

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Learning and memory impairment in rats with chronic atypical absence seizures

Cited by 50 publications

References 57 publications

Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies

Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies

Temporal current-source of spikes suggests initial treatment failure in childhood absence epilepsy

Choosing the Correct Antiepileptic Drugs: From Animal Studies to the Clinic

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