Electroconvulsive Thresholds of Inbred Mouse Strains

Frankel, Wayne N.; Taylor, Laura J.; Beyer, Barbara; Tempel, Bruce L.; White, H. Steve

doi:10.1006/geno.2001.6564

Cited by 120 publications

(121 citation statements)

References 13 publications

Supporting

Mentioning

112

Contrasting

Unclassified

Order By: Relevance

“…Three standard transcorneal electroconvulsive seizure paradigms were applied to determine hindbrain, forebrain, and limbic seizure thresholds (Barton, et al, 2001;Frankel, et al, 2001;Otto, et al, 2004). All testing was conducted January -February, 12pm -6pm.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Strain and age affect electroconvulsive seizure testing in rats

2008

View full text Add to dashboard Cite

SummaryElectroconvulsive seizure thresholds were compared between adolescent and mature SpragueDawley, Wistar, and Fischer rats. All strains had similar hindbrain or forebrain seizure thresholds as adolescents. As adults, hindbrain or forebrain seizure thresholds were highest for Sprague-Dawley and lowest for Fischer rats. Conversely, limbic seizure thresholds during adolescence were highest for Fischer rats. Additional study is needed to better delineate strain and maturational effects on electroconvulsive seizure testing.

show abstract

Section: Methodsmentioning

confidence: 99%

“…Mouse strain influences electroconvulsive seizure thresholds (Frankel, et al, 2001), but data in rats are lacking. We compared adolescent and adult electroconvulsive seizure thresholds for Sprague-Dawley, Wistar, and Fischer rats.…”

Section: Introductionmentioning

confidence: 99%

Strain and age affect electroconvulsive seizure testing in rats

2008

View full text Add to dashboard Cite

show abstract

“…The NIH-sponsored mutagenesis center at the Jackson Laboratory is screening for mutations that decrease the threshold for seizures after electroconvulsive shock (31). Already several seizure-prone models have emerged (e.g., http://www.jax.org/resources/documents/nmf/), and all mutants will be available to interested investigators.…”

Section: New Monogenic Epilepsies From Large-scale Chemical Mutagenesmentioning

confidence: 99%

Identification of Epilepsy Genes in Human and Mouse

et al. 2001

View full text Add to dashboard Cite

The development of molecular markers and genomic resources has facilitated the isolation of genes responsible for rare monogenic epilepsies in human and mouse. Many of the identified genes encode ion channels or other components of neuronal signaling. The electrophysiological properties of mutant alleles indicate that neuronal hyperexcitability is one cellular mechanism underlying seizures. Genetic heterogeneity and allelic variability are hallmarks of human epilepsy. For example, mutations in three different sodium channel genes can produce the same syndrome, GEFS+, while individuals with the same allele can experience different types of seizures. Haploinsufficiency for the sodium channel SCN1A has been demonstrated by the severe infantile epilepsy and cognitive deficits in heterozygotes for de novo null mutations. Large-scale patient screening is in progress to determine whether less severe alleles of the genes responsible for monogenic epilepsy may contribute to the common types of epilepsy in the human population. The development of pharmaceuticals directed towards specific epilepsy genotypes can be anticipated, and the introduction of patient mutations into the mouse genome will provide models for testing these targeted therapies.

show abstract

“…To quantify changes in seizure threshold produced by TBI, and to deliver a controlled second-hit, we allowed mice to recover for 7 days before administering an electroconvulsive shock (ECS), a well-established method for seizure induction in the rodent (Ferraro et al, 2002;Frankel et al, 2001). As an initial step toward determining the mechanisms by which activated astrocytes affect neuronal function, we measured changes in the zinc binding protein metallothionein, which is released from astrocytes in response to neuronal injury (Chung et al, 2004).…”

mentioning

confidence: 99%

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Chrzaszcz

Venkatesan

Dragisic

et al. 2010

Journal of Neurotrauma

View full text Add to dashboard Cite

The mechanisms linking traumatic brain injury (TBI) to post-traumatic epilepsy (PTE) are not known and no therapy for prevention of PTE is available. We used a mouse closed-skull midline impact model to test the hypotheses that TBI increases susceptibility to seizures in a ''two-hit'' injury model, and that suppression of cytokine upregulation after the first hit will attenuate the increased susceptibility to the second neurological insult. Adult male CD-1 mice underwent midline closed skull pneumatic impact. At 3 and 6 h after impact or sham procedure, the mice were injected IP with either Minozac (Mzc), a suppressor of proinflammatory cytokine upregulation, or vehicle (saline). On day 7 after sham operation or TBI, seizures were induced using electroconvulsive shock (ECS), and susceptibility to seizures was measured by the current required for seizure induction. Activation of glia, neuronal injury, and metallothionein-immunoreactive cells were quantified in the hippocampus by immunohistochemical methods. Neurobehavioral function over 14-day recovery was quantified using the Barnes maze. Following TBI there was a significant increase in susceptibility to seizures induced by ECS, and this susceptibility was prevented by suppression of cytokine upregulation with Mzc. Astrocyte activation, metallothionein expression, and neurobehavioral impairment were also increased in the two-hit group subjected to combined TBI and ECS. These enhanced responses in the two-hit group were also prevented by suppression of proinflammatory cytokine upregulation with Mzc. These data implicate glial activation in the mechanisms of epileptogenesis after TBI, and identify a potential therapeutic approach to attenuate the delayed neurological sequelae of TBI.

show abstract

Electroconvulsive Thresholds of Inbred Mouse Strains

Cited by 120 publications

References 13 publications

Strain and age affect electroconvulsive seizure testing in rats

Strain and age affect electroconvulsive seizure testing in rats

Identification of Epilepsy Genes in Human and Mouse

Minozac Treatment Prevents Increased Seizure Susceptibility in a Mouse “Two-Hit” Model of Closed Skull Traumatic Brain Injury and Electroconvulsive Shock-Induced Seizures

Contact Info

Product

Resources

About