Elevated anxiety and depressive-like behavior in a rat model of genetic generalized epilepsy suggesting common causation

Jones, Nigel C.; Salzberg, Michael; Kumar, Gaurav; Couper, Abbie; Morris, Margaret J.; O’Brien, Terence J.

doi:10.1016/j.expneurol.2007.09.026

Cited by 178 publications

(151 citation statements)

References 35 publications

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“…The forced swimming test (FST) was designed as a primary screening test for antidepressants, but the sensitivity of the FST in detecting TBI-induced depression has not been consistent. Although depression-like behavior during the FST has been reported previously in a mild TBI model using weight drop (Milman et al, 2005;Shapira et al, 2007), it was not detected in our current mouse TBI model, or in the fluid-percussion injury model ( Jones et al, 2008). Potential contributing factors to the differential detection of depression-like behavior by FST after brain injury may lie in differences in the models and severity of experimental TBI, the timing of the affective measures used following injury, and/or other methodological differences.…”

Section: Figcontrasting

confidence: 40%

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Wang

Neumann

Hansen

et al. 2011

Journal of Neurotrauma

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The selective serotonin reuptake inhibitor fluoxetine induces hippocampal neurogenesis, stimulates maturation and synaptic plasticity of adult hippocampal neurons, and reduces motor/sensory and memory impairments in several CNS disorders. In the setting of traumatic brain injury (TBI), its effects on neuroplasticity and function have yet to be thoroughly investigated. Here we examined the efficacy of fluoxetine after a moderate to severe TBI, produced by a controlled cortical impact. Three days after TBI or sham surgery, mice were treated with fluoxetine (10 mg/kg/d) or vehicle for 4 weeks. To evaluate the effects of fluoxetine on neuroplasticity, hippocampal neurogenesis and epigenetic modification were studied. Stereologic analysis of the dentate gyrus revealed a significant increase in doublecortin-positive cells in brain-injured animals treated with fluoxetine relative to controls, a finding consistent with enhanced hippocampal neurogenesis. Epigenetic modifications, including an increase in histone 3 acetylation and induction of methyl-CpG-binding protein, a transcription factor involved in DNA methylation, were likewise seen by immunohistochemistry and quantitative Western immunoblots, respectively, in brain-injured animals treated with fluoxetine. To determine if fluoxetine improves neurological outcomes after TBI, gait function and spatial learning and memory were assessed by the CatWalkassisted gait test and Barnes maze test, respectively. No differences in these parameters were seen between fluoxetine-and vehicle-treated animals. Thus while fluoxetine enhanced neuroplasticity in the hippocampus after TBI, its chronic administration did not restore locomotor function or ameliorate memory deficits.

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Section: Figcontrasting

confidence: 40%

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Wang

Neumann

Hansen

et al. 2011

Journal of Neurotrauma

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“…The possible explanation can be based on the correlation between seizure intensity and duration. The results from our study do not significantly deviate from these findings, meaning that this model is suitable for the further research of this phenomenon (8,(13)(14)(15).…”

Section: Discussioncontrasting

confidence: 37%

“…Many studies have been using different models for inducing epilepsy in experimental animals, in order to examine correlation between epilepsy and its comorbidities. Interestingly, no matter if the experimental animals were being genetically prone to the epileptic seizures (13), or if the bilateral or unilateral kindling, the decreased levels of exploration were always noticed, as a method in inducing the seizures were used (14), further leading to the possible conclusion of the presence of anxiety-related behavior (15). On the other hand, the decrease of the exploration-prone behavioral pattern of rats, differs from one study to another.…”

Section: Discussionmentioning

confidence: 99%

Exploratory behavior alteration as an epileptic comorbidity in elevated plus maze test

Ademovič¹,

Lekovic²,

Knežević³

et al. 2017

Med podmladak

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Introduction: Epileptic seizure consists of preictal, ictal and postictal period. Postictal period is characterized by a variety of psychiatric phenomenon of which the most frequent ones are anxiety and depressive disorder. Anxiety in rodents can be assessed by measuring the exploratory behavior. Lindane evokes generalized tonic-clonic epileptic seizures in rats, when applied intraperitoneally, due to its lypophilic characteristics. Aim: The aim of this study was to assess exploratory behavior linked with anxiety level in the elevated plus maze test (EPM) upon generalized seizures, induced by lindane in male rats. Material and methods: The experiment was conducted on Wistar albino male rats that were randomly divided into: control group (DMSO, 0.5 ml/kg) and experimental group (lindane, 8 mg/kg) (n=8, each). After the drug injection, the assessment of the seizure intensity lasted for 30 minutes. Descriptive rating scale was used to describe the seizure severity. Subsequently, the EPM testing took place immediately after evoking the seizure (Test 1), after 1h (Test 2) and after 24h (Test 3). Time spent in open areas and number of transitions was further analyzed. Results: Experimental group of animals spent less time in open areas of EPM, when compared to controls in Test 1 and Test 2. The same holds true for the number of transitions to the open area, i.e. lindane-treated animals tend to stay in enclosed parts of the maze in Test1, Test 2. Finally, in Test 3 there was no significant difference between the groups, in any parameter of interest. Conclusion: Lindane-induced generalized epileptic seizures are accompanied by reduced exploratory behavior in the elevated plus maze test, up to 24h after the seizure ended. This finding can be a basis for the further translational research of anxiety as epileptic comorbidity in this experimental model of epilepsy.

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“…An important finding is that the development of anxiety was already detectable before the onset of epilepsy. This is an especially important paper as it suggests a common pathophysiological basis of epilepsy and anxiety rather than explaining anxiety as a secondary (neurodegenerative or psychosocial) consequence of epilepsy and seizures (Jones et al, 2008).…”

Section: Neurobiological Correlatesmentioning

confidence: 99%

Anxiety disorders in people with epilepsy

Brandt¹,

Mula

2016

Epilepsy & Behavior

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Anxiety disorders are frequent, though probably underdiagnosed comorbidities in epilepsy.Epilepsy and anxiety may share common neurobiological correlates as shown in animal models and suggested by studies demonstrating anxiety disorders before the manifestation of epilepsy. Comorbid anxiety disorders have a major impact on the affected patients' qualityof-life and may increase the risk for suicidality. Successful treatment of the epilepsy may alleviate anxiety symptoms. Treatment of anxiety is based on selective serotonin reuptake inhibitors, benzodiazepines (although only further choice) and psychotherapy. Specific AEDs (especially pregabalin) have been shown to have anxiolytic properties. This paper is aimed at reviewing anxiety disorders in patients with epilepsy discussing current scientific evidence about pathophysiology, clinical aspects and treatment strategies.

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Elevated anxiety and depressive-like behavior in a rat model of genetic generalized epilepsy suggesting common causation

Cited by 178 publications

References 35 publications

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Exploratory behavior alteration as an epileptic comorbidity in elevated plus maze test

Anxiety disorders in people with epilepsy

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