The systemic kainic acid rat model of temporal lobe epilepsy: Long-term EEG monitoring

Nieuwenhuyse, Bregt Van; Raedt, Robrecht; Sprengers, Mathieu; Dauwe, Ine; Gadeyne, Stefanie; Carrette, Evelien; Delbeke, Jean; Wadman, Wytse J.; Boon, Paul; Vonck, Kristl

doi:10.1016/j.brainres.2015.08.016

Cited by 57 publications

(72 citation statements)

References 44 publications

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“…Moreover, it is not established if this model may mimic at least some pathophysiological features of the most diffused type of refractory epilepsy, i.e., temporal lobe epilepsy (TLE; Curia et al, 2014). For instance, a prominent feature of TLE models is the presence of a process named “secondary epileptogenesis” (Williams et al, 2009; Pitkänen and Lukasiuk, 2011; Löscher et al, 2015; Van Nieuwenhuyse et al, 2015), by which a progressive aggravation of seizures occurs in epileptic animals.…”

Section: Introductionmentioning

confidence: 99%

Progressive Seizure Aggravation in the Repeated 6-Hz Corneal Stimulation Model Is Accompanied by Marked Increase in Hippocampal p-ERK1/2 Immunoreactivity in Neurons

Giordano

Costa

Lucchi

et al. 2016

Front. Cell. Neurosci.

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The 6-Hz corneal stimulation test is used to screen novel antiepileptic molecules to overcome the problem of drug refractoriness. Although recognized as a standard test, it has been evaluated only recently in the attempt to characterize the putative neuronal networks involved in seizures caused by corneal stimulation. In particular, by recording from the CA1 region we previously established that the hippocampus participates to propagation of seizure activity. However, these findings were not corroborated by using markers of neuronal activation such as FosB/ΔFosB antigens. In view of this discrepancy, we performed new experiments to characterize the changes in levels of phosphorylated extracellular signal-regulated kinases1/2 (p-ERK1/2), which are also used as markers of neuronal activation. To this aim, mice underwent corneal stimulation up to three different times, in three sessions separated by an interval of 3 days. To characterize a group in which seizures could be prevented by pharmacological treatment, we also considered pretreatment with the ghrelin receptor antagonist EP-80317 (330 μg/kg). Control mice were sham-treated. Video electrocorticographic (ECoG) recordings were obtained from mice belonging to each group of treatment. Animals were finally used to characterize the immunoreactivity for FosB/ΔFosB and p-ERK1/2 in the hippocampus. As previously shown, FosB/ΔFosB levels were highly increased throughout the hippocampus by the first induced seizure but, in spite of the progressively increased seizure severity, they were restored to control levels after the third stimulation. At variance, corneal stimulation caused a progressive increase in p-ERK1/2 immunoreactivity all over the hippocampus, especially in CA1, peaking in the third session. Predictably, EP-80317 administration reduced both duration and severity of seizures, prevented the increase in FosB/ΔFosB levels in the first session, and partially counteracted the increase in p-ERK1/2 levels in the third session. The vast majority of p-ERK1/2 immunopositive cells were co-labeled with FosB/ΔFosB antibodies, suggesting the existence of a relationship between the investigated markers in a subpopulation of neurons activated by seizures. These findings suggest that p-ERK1/2 are useful markers to define the aggravation of seizures and the response to anticonvulsant treatments. In particular, p-ERK1/2 expression clearly identified the involvement of hippocampal regions during seizure aggravation in the 6-Hz model.

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Section: Introductionmentioning

confidence: 99%

Progressive Seizure Aggravation in the Repeated 6-Hz Corneal Stimulation Model Is Accompanied by Marked Increase in Hippocampal p-ERK1/2 Immunoreactivity in Neurons

Giordano

Costa

Lucchi

et al. 2016

Front. Cell. Neurosci.

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“…Kainic acid is a glutamate derivative and its single systemic injection to rodents results in seizures, neuroinflammation, and neuronal degeneration or death on selective population of neurons in the brain. [20][21][22] These pathological alternations are similar to human temporal lobe epilepsy. 23,24) Administering kainic acid to rodents is generally considered to induce an adequate model of epilepsy.…”

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confidence: 66%

Echinacoside, an Active Constituent of <i>Cistanche Herba</i>, Exerts a Neuroprotective Effect in a Kainic Acid Rat Model by Inhibiting Inflammatory Processes and Activating the Akt/GSK3β Pathway

Hsieh

Lin

et al. 2018

Biological & Pharmaceutical Bulletin

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Echinacoside is a major compound of Cistanche Herb and has glutamate release-inhibiting activity in the brain. Given the involvement of excitotoxicity caused by massive glutamate in the pathophysiology of epilepsy, we explored the antiepileptic effect of echinacoside on kainic acid-induced seizures in rats. The rats were intraperitoneally administrated echinacoside for 30 min prior to intraperitoneal injection with kainic acid. The results showed that kainic acid induced seizure-like behavioral patterns, increased glutamate concentrations, caused neuronal loss and microglial activation, and stimulated proinflammatory cytokine gene expression in the hippocampus. These kainic acid-induced alternations were found to be attenuated by echinacoside pretreatment. Furthermore, decreased Akt and glycogen synthase kinase 3β (GSK3β) phosphorylation as well as Bcl-2 expression in the hippocampus was reversed by the echinacoside pretreatment. These results demonstrate that echinacoside exert its antiepileptic and neuroprotective actions in a kainic acid rat model through suppressing inflammatory response and activating the Akt/GSK3β signaling. Therefore, the present study suggests that echinacoside is the potentially useful in the prevention of epilepsy.

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“…During ictal and interictal periods, there are over-synchronized discharges in the cerebral cortex [21]. Furthermore, it has been shown that EEG recordings demonstrate that kainic acid-induced epilepsy is a useful model for epilepsy research [22]. …”

Section: Discussionmentioning

confidence: 99%

Dynamic expression of CX36 protein in kainic acid kindling induced epilepsy

Wang

Hao

et al. 2017

Translational Neuroscience

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Connexin (Cx) 36 is known to be a component of gap junctions, and has been suggested to play an important role in epilepsy. In order to determine dynamic changes of Cx36 protein expression in epilepsy and investigate the role of Cx36 in electroencephalographic activity and pathogenesis, we utilized kainic acid (KA) to induce epileptogenesis. We found that epileptic discharges began 71.8 ± 23.7 s after KA administration. Spike frequency and amplitude of epileptiform activity reached maximal levels at 30 ± 5.2 min. The maximum level of spike frequency and amplitude of epileptiform activity was 13.9 ± 0.3 Hz and 198 ± 14.3mV respectively. Employing Western blotting and immunohistochemistry, we demonstrated that hippocampal Cx36 protein expression was significantly increased 6 h after KA kindling compared to control or sham groups, but decreased in 3 d and 7d groups. Our results suggested that the dynamic change of Cx36 expression may play an important role inepilepsy, and the specific manipulation of Cx36 expression may be a potential target for the treatment of epilepsy.

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The systemic kainic acid rat model of temporal lobe epilepsy: Long-term EEG monitoring

Cited by 57 publications

References 44 publications

Progressive Seizure Aggravation in the Repeated 6-Hz Corneal Stimulation Model Is Accompanied by Marked Increase in Hippocampal p-ERK1/2 Immunoreactivity in Neurons

Progressive Seizure Aggravation in the Repeated 6-Hz Corneal Stimulation Model Is Accompanied by Marked Increase in Hippocampal p-ERK1/2 Immunoreactivity in Neurons

Echinacoside, an Active Constituent of <i>Cistanche Herba</i>, Exerts a Neuroprotective Effect in a Kainic Acid Rat Model by Inhibiting Inflammatory Processes and Activating the Akt/GSK3β Pathway

Dynamic expression of CX36 protein in kainic acid kindling induced epilepsy

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