Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

Kelly, Kenneth G.; Miller, Eric R.; Lepsveridze, Eka; Kharlamov, Elena A.; Mchedlishvili, Zakaria

doi:10.1016/j.eplepsyres.2015.09.009

Cited by 49 publications

(36 citation statements)

References 66 publications

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“…However, as in the studies in mice, these SLEs in rats were clearly different in several aspects, including morphology, incidence, and frequency, from those in models of acquired epilepsy in rats 33, 34, 40. In addition to the possibility that such SLEs in sham controls are a consequence of depth‐electrode‐induced lesions, inherent 8‐ to 11‐Hz spike‐wave discharges (SWDs) are commonly recorded in both inbred and outbred rat strains, but these SWDs are easily distinguished from lesion‐induced ictal discharges in models of traumatic brain injury 41. Spontaneous SWDs (or other types of nonconvulsive seizures) do not occur in most inbred and outbred mouse strains, including those used in the present study,42 but 6‐ to 8‐Hz SWDs have been described in some inbred strains such as DBA/2, C3H/HeJ, and A/J 42, 43, 44.…”

Section: Discussionmentioning

confidence: 99%

“…33,34,40 In addition to the possibility that such SLEs in sham controls are a consequence of depthelectrode-induced lesions, inherent 8-to 11-Hz spike-wave discharges (SWDs) are commonly recorded in both inbred and outbred rat strains, but these SWDs are easily distinguished from lesion-induced ictal discharges in models of traumatic brain injury. 41 Spontaneous SWDs (or other types of nonconvulsive seizures) do not occur in most inbred and outbred mouse strains, including those used in the present study, 42 but 6-to 8-Hz SWDs have been described in some inbred strains such as DBA/2, C3H/HeJ, and A/J. [42][43][44] Interestingly, in male sham NMRI control mice with depth electrode in the hippocampus, no HVSW-or HPD-like EEG activity was observed but only some infrequent spikes (F. Twele, unpublished data).…”

Section: Not Applicable Not Applicablementioning

confidence: 99%

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The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

Twele¹,

Töllner²,

Bankstahl³

et al. 2016

Epilepsia Open

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SummaryObjectiveMesial temporal lobe epilepsy (TLE) with hippocampal sclerosis is a predominant form of acquired epilepsy, characterized by recurrent simple and complex partial seizures that are often resistant to treatment. Mice developing spontaneous recurrent nonconvulsive and convulsive seizures after intrahippocampal injection of the excitotoxic glutamate agonist kainate are thought to represent a valuable model of mesial TLE. Epileptic electroencephalogram (EEG) activity recorded in this model from the kainate focus in the ipsilateral hippocampus is resistant to antiseizure drugs such as carbamazepine (CBZ). We compared the efficacy of CBZ in this model in two different mouse strains (FVB/N and NMRI). Furthermore, we evaluated whether changes in the definition of electrographic seizures affect the antiseizure efficacy of CBZ.MethodsAs in previous studies, two types of epileptic EEG activity were defined: high‐voltage sharp waves (HVSWs) and hippocampal paroxysmal discharges (HPDs). The characteristics of these paroxysmal EEG events in epileptic mice were compared with EEG criteria for nonconvulsive seizures in patients. For HVSWs, different spike frequencies, interevent intervals, and amplitudes were used as inclusion and exclusion criteria. In addition to CBZ, some experiments were performed with diazepam (DZP) and phenobarbital (PB).ResultsFemale epileptic FVB/N mice predominantly exhibited frequent HVSWs, but only infrequent HPDs or secondarily generalized convulsive seizures. Slight changes in HVSW definition determined whether they were resistant or responsive to CBZ. Male NMRI mice exhibited both HVSWs and HPDs. HVSWs were more resistant than HPDs to suppression by CBZ. Both types of epileptic EEG activity were rapidly suppressed by DZP and PB.SignificanceThe data demonstrate that focal electrographic seizures in the intrahippocampal kainate mouse model are less resistant than previously thought. Both mouse strain and the criteria chosen for definition of EEG seizures determine whether such seizures are drug‐resistant or ‐responsive.

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Section: Discussionmentioning

confidence: 99%

Section: Not Applicable Not Applicablementioning

confidence: 99%

The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

Twele¹,

Töllner²,

Bankstahl³

et al. 2016

Epilepsia Open

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show abstract

“…It is possible that the increased regeneration can even result in adverse effects. For example, sprouting of mossy fibers following TBI has been suggested to result in epilepsy [43][44][45]. In contrast to the increased synaptogenesis, our quantification of DCX positive cells, showed that there is no longterm effect on neurogenesis following TBI in the tg-ArcSwe mice.…”

Section: Discussionmentioning

confidence: 58%

Long-Term Effects of Traumatic Brain Injury in a Mouse Model of Alzheimer’s Disease

Zyśk

Clausen

Aguilar

et al. 2019

JAD

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Alzheimer's disease (AD) is the leading cause of dementia worldwide, affecting over 10% of the elderly population. Epidemiological evidence indicates that traumatic brain injury (TBI) is an important risk factor for developing AD later in life. However, which injury-induced processes that contribute to the disease onset remains unclear. The aim with the present study was to identify cellular processes that could link TBI to AD development, by investigating the chronic impact of two different injury models, controlled cortical impact (CCI) and midline fluid percussion injury (mFPI). The trauma was induced in 3-month-old tg-ArcSwe mice, carrying the Arctic mutation along with the Swedish mutation, and the influence of TBI on AD progression was analyzed at 12-and 24-weeks post-injury. The long-term effect of the TBI on memory deficiency, amyloid-␤ (A␤) pathology, neurodegeneration and inflammation was investigated by Morris water maze, PET imaging, immunohistochemistry, and biochemical analyses. Morris water maze analysis demonstrated that mice subjected to CCI or mFPI performed significantly worse than uninjured tg-ArcSwe mice, especially at the later time point. Moreover, the injured mice showed a late upregulation of reactive gliosis, which concurred with a more pronounced A␤ pathology, compared to uninjured AD mice. Our results suggest that the delayed glial activation following TBI may be an important link between the two diseases. However, further studies in both experimental models and human TBI patients will be required to fully elucidate the reasons why TBI increases the risk of neurodegeneration.

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“…This post-traumatic epilepsy (PTE) has a reported incidence of up to 35% after severe TBI (Annegers et al, 1980;Ates et al, 2006;Arndt et al, 2013). While several wellcharacterized experimental models have been utilized in adult rodents to explore PTE after TBI to the mature brain (D'ambrosio et al, 2004;Bolkvadze and Pitkanen, 2012;Kelly et al, 2015;Ostergard et al, 2016), there has been a lack of ageappropriate models to consider the complex interaction between ongoing brain development and epileptogenesis that occurs after a TBI during early childhood.…”

Section: Early Life Neurotraumamentioning

confidence: 99%

Immune Challenges and Seizures: How Do Early Life Insults Influence Epileptogenesis?

2020

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The development of epilepsy, a process known as epileptogenesis, often occurs later in life following a prenatal or early postnatal insult such as cerebral ischemia, stroke, brain trauma, or infection. These insults share common pathophysiological pathways involving innate immune activation including neuroinflammation, which is proposed to play a critical role in epileptogenesis. This review provides a comprehensive overview of the latest preclinical evidence demonstrating that early life immune challenges influence neuronal hyperexcitability and predispose an individual to later life epilepsy. Here, we consider the range of brain insults that may promote the onset of chronic recurrent spontaneous seizures at adulthood, spanning intrauterine insults (e.g. maternal immune activation), perinatal injuries (e.g. hypoxic-ischemic injury, perinatal stroke), and insults sustained during early postnatal life-such as fever-induced febrile seizures, traumatic brain injuries, infections, and environmental stressors. Importantly, all of these insults represent, to some extent, an immune challenge, triggering innate immune activation and implicating both central and systemic inflammation as drivers of epileptogenesis. Increasing evidence suggests that pro-inflammatory cytokines such as interleukin-1 and subsequent signaling pathways are important mediators of seizure onset and recurrence, as well as neuronal network plasticity changes in this context. Our current understanding of how early life immune challenges prime microglia and astrocytes will be explored, as well as how developmental age is a critical determinant of seizure susceptibility. Finally, we will consider the paradoxical phenomenon of preconditioning, whereby these same insults may conversely provide neuroprotection. Together, an improved appreciation of the neuroinflammatory mechanisms underlying the long-term epilepsy risk following early life insults may provide insight into opportunities to develop novel immunological antiepileptogenic therapeutic strategies.

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Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

Cited by 49 publications

References 66 publications

The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

The effects of carbamazepine in the intrahippocampal kainate model of temporal lobe epilepsy depend on seizure definition and mouse strain

Long-Term Effects of Traumatic Brain Injury in a Mouse Model of Alzheimer’s Disease

Immune Challenges and Seizures: How Do Early Life Insults Influence Epileptogenesis?

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