Relation between startle reactivity and sucrose avidity in two rat strains bred for differential seizure susceptibility

Runke, Dwayne; McIntyre, Dan C.; St-Onge, Veronique; Gilby, Krista L.

doi:10.1016/j.expneurol.2011.02.006

Cited by 8 publications

(3 citation statements)

References 53 publications

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“…Many investigators are currently interested in shared causes of epilepsy and comorbidities. Supporting the case for a shared causation between the epilepsy and psychiatric comorbidities, rat strains that have an increased predisposition to developing epilepsy following a brain insult (but are not epileptic initially), such as the FAST rats (a strain where kindling occurs rapidly) and genetically epilepsy prone rats (GEPRs), show a range of behavioral phenotypes relevant to the psychiatric comorbidities of patients with epilepsy (Anisman & McIntyre, ; McIntyre et al., ; Jobe & Weber, ; Gilby et al., Runke et al., ). In mouse models of Alzheimer's disease (AD), which often exhibit recurrent seizures and therefore have epilepsy (Palop et al., ; Minkeviciene et al., ; Scharfman, ), cognitive impairments that accompany seizures may be due to similar mechanisms as the seizures.…”

Section: Animal Models To Study Comorbidities Of Epilepsymentioning

confidence: 99%

Issues related to symptomatic and disease‐modifying treatments affecting cognitive and neuropsychiatric comorbidities of epilepsy

et al. 2013

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Summary Many symptoms of neurologic or psychiatric illness—such as cognitive impairment, depression, anxiety, attention deficits, and migraine—occur more frequently in people with epilepsy than in the general population. These diverse comorbidities present an underappreciated problem for people with epilepsy and their caregivers because they decrease quality of life, complicate treatment, and increase mortality. In fact, it has been suggested that comorbidities can have a greater effect on quality of life in people with epilepsy than the seizures themselves. There is increasing recognition of the frequency and impact of cognitive and behavioral comorbidities of epilepsy, highlighted in the 2012 Institute of Medicine report on epilepsy. Comorbidities have also been acknowledged, as a National Institutes of Health (NIH) Benchmark area for research in epilepsy. However, relatively little progress has been made in developing new therapies directed specifically at comorbidities. On the other hand, there have been many advances in understanding underlying mechanisms. These advances have made it possible to identify novel targets for therapy and prevention. As part of the International League Against Epilepsy/American Epilepsy Society workshop on preclinical therapy development for epilepsy, our working group considered the current state of understanding related to terminology, models, and strategies for therapy development for the comorbidities of epilepsy. Herein we summarize our findings and suggest ways to accelerate development of new therapies. We also consider important issues to improve research including those related to methodology, nonpharmacologic therapies, biomarkers, and infrastructure.

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Section: Animal Models To Study Comorbidities Of Epilepsymentioning

confidence: 99%

Issues related to symptomatic and disease‐modifying treatments affecting cognitive and neuropsychiatric comorbidities of epilepsy

et al. 2013

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“…Acoustic startle reaction. The genetic basis of differences in startle reaction in strains, which differ in AE-proneness and/or in defense reactions, was also shown [ 25 , 82 , 83 ]. The precise location of the chromosome fragment in mice was indicated, which is responsible for pinch-induced catalepsy [ 56 ].…”

Section: Genetics Of Aementioning

confidence: 99%

Rodent Brain Pathology, Audiogenic Epilepsy

et al. 2021

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The review presents data which provides evidence for the internal relationship between the stages of rodent audiogenic seizures and post-ictal catalepsy with the general pattern of animal reaction to the dangerous stimuli and/or situation. The wild run stage of audiogenic seizure fit could be regarded as an intense panic reaction, and this view found support in numerous experimental data. The phenomenon of audiogenic epilepsy probably attracted the attention of physiologists as rodents are extremely sensitive to dangerous sound stimuli. The seizure proneness in this group shares common physiological characteristics and depends on animal genotype. This concept could be the new platform for the study of epileptogenesis mechanisms.

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“…Standard amygdala or hippocampal kindling did not produce differences in immobility in the FST or preference for sucrose in rats [31, 32]. FAST rats, which were selectively bred for accelerated amygdala kindling and showed a variety of anxiety-related phenotypes, actually had increased sucrose preference versus their SLOW kindling counterparts [33]. However, rapid kindling of the ventral hippocampus increased immobility in the FST and decreased saccharin preference, suggestive of a depressive-like phenotype [34].…”

Section: Existing Animal Models Of Depression and Epilepsy Comorbimentioning

confidence: 99%

Rhythm and blues: Animal models of epilepsy and depression comorbidity

Epps

Weinshenker

2013

Biochemical Pharmacology

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Clinical evidence shows a strong, bidirectional comorbidity between depression and epilepsy that is associated with decreased quality of life and responsivity to pharmacotherapies. At present, the neurobiological underpinnings of this comorbidity remain hazy. To complicate matters, anticonvulsant drugs can cause mood disturbances, while antidepressant drugs can lower seizure threshold, making it difficult to treat patients suffering from both depression and epilepsy. Animal models have been created to untangle the mechanisms behind the relationship between these disorders and to serve as screening tools for new therapies targeted to treat both simultaneously. These animal models are based on chemical interventions (e.g. pentylenetetrazol, kainic acid, pilocarpine), electrical stimulations (e.g. kindling, electroshock), and genetic/selective breeding paradigms (e.g. Genetically Epilepsy-Prone Rats (GEPRs), Genetic Absence Epilepsy Rat from Strasbourg (GAERS), WAG/Rij rats, Swim Lo-Active rats (SwLo)). Studies on these animal models point to some potential mechanisms that could explain epilepsy and depression comorbidity, such as various components of the dopaminergic, noradrenergic, serotonergic, and GABAergic systems, as well as key brain regions, like the amygdala and hippocampus. These models have also been used to screen possible therapies. The purpose of the present review is to highlight the importance of animal models in research on comorbid epilepsy and depression and to explore the contributions of these models to our understanding of the mechanisms and potential treatments for these disorders.

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Relation between startle reactivity and sucrose avidity in two rat strains bred for differential seizure susceptibility

Cited by 8 publications

References 53 publications

Issues related to symptomatic and disease‐modifying treatments affecting cognitive and neuropsychiatric comorbidities of epilepsy

Issues related to symptomatic and disease‐modifying treatments affecting cognitive and neuropsychiatric comorbidities of epilepsy

Rodent Brain Pathology, Audiogenic Epilepsy

Rhythm and blues: Animal models of epilepsy and depression comorbidity

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