Acute and spontaneous seizure onset zones in the intraperitoneal kainic acid model

Connell, Phillip; Bayat, Arezou; Joshi, Sumit; Koubeissi, Mohamad Z.

doi:10.1016/j.yebeh.2016.12.017

Cited by 14 publications

(8 citation statements)

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“…The consistency of a duration effect for KA, pilocarpine, as well as the gain‐ versus loss‐of‐function models, suggests that adult‐born neurons have their influence mainly by lengthening or curtailing seizures rather than facilitating or blocking the initiation of SE. This influence is consistent with the idea that after KA or pilocarpine, seizures can be initiated in areas outside the DG (Botterill, LaFrancois, & Scharfman, ; Connell, Bayat, Joshi, & Koubeissi, ). The idea is also consistent with the view that the DG is an inhibitory brake on seizures that already have been generated in cortex and are propagating into the DG (Bonislawski, Schwarzbach, & Cohen, ; Dengler & Coulter, ; Heinemann et al, ; Hsu, ; Krook‐Magnuson et al, ; Lothman, Stringer, & Bertram, ; Pathak et al, ; Patrylo, Tyagi, Willingham, Lee, & Williamson, ; Scharfman & Myers, ).…”

Section: Discussionsupporting

confidence: 90%

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

et al. 2019

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Previous studies suggest that reducing the numbers of adult‐born neurons in the dentate gyrus (DG) of the mouse increases susceptibility to severe continuous seizures (status epilepticus; SE) evoked by systemic injection of the convulsant kainic acid (KA). However, it was not clear if the results would be the same for other ways to induce seizures, or if SE‐induced damage would be affected. Therefore, we used pilocarpine, which induces seizures by a different mechanism than KA. Also, we quantified hippocampal damage after SE. In addition, we used both loss‐of‐function and gain‐of‐function methods in adult mice. We hypothesized that after loss‐of‐function, mice would be more susceptible to pilocarpine‐induced SE and SE‐associated hippocampal damage, and after gain‐of‐function, mice would be more protected from SE and hippocampal damage after SE. For loss‐of‐function, adult neurogenesis was suppressed by pharmacogenetic deletion of dividing radial glial precursors. For gain‐of‐function, adult neurogenesis was increased by conditional deletion of pro‐apoptotic gene Bax in Nestin‐expressing progenitors. Fluoro‐Jade C (FJ‐C) was used to quantify neuronal injury and video‐electroencephalography (video‐EEG) was used to quantify SE. Pilocarpine‐induced SE was longer in mice with reduced adult neurogenesis, SE had more power and neuronal damage was greater. Conversely, mice with increased adult‐born neurons had shorter SE, SE had less power, and there was less neuronal damage. The results suggest that adult‐born neurons exert protective effects against SE and SE‐induced neuronal injury.

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Section: Discussionsupporting

confidence: 90%

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

et al. 2019

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“…KA could induce robust depolarizations and even cell death 27–29 and many studies successfully mapped the localization of KA receptors 30 . KA receptors express at different levels in entorhinal cortex 31–33 , cerebellum 34 , amygdale 35 and basal ganglia 11,36 .…”

Section: Discussionmentioning

confidence: 99%

Stereotypical patterns of epileptiform calcium signal in hippocampal CA1, CA3, dentate gyrus and entorhinal cortex in freely moving mice

Zhang

Qiao

Liu

et al. 2019

Sci Rep

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Epilepsy is a multi-etiological brain dysfunction syndrome. Hippocampal neuronal damage induced by seizures may be one of the causes leading to cognitive impairment, but the underlying mechanism remains to be further elucidated. The kainic acid (KA) model of temporal lobe epilepsy is widely used in understanding of the epileptogenesis. Fiber photometry is a signal detection technology suitable for recording calcium activity of neurons in the deep brain of freely moving animal. Here, we used the optical fiber-based method to monitor the real-time neuronal population activities of freely moving mice after subcutaneous injection of KA. We observed that KA administration led to one to three kinds of stereotypical patterns of epileptiform calcium activity in CA1, CA3, and dentate gyrus (DG) of the hippocampus, as well as the entorhinal cortex (EC). There were three kinds of waves in the hippocampal CA1, which we named wave 1, wave 2 and slow flash. Wave 1 and wave 2 appeared in both the CA3 and DG regions, but the EC only showed wave 1. In these epileptiform calcium signals, we observed a high amplitude and long duration calcium wave as a part of wave 2, which resembled cortical spreading depression (CSD) and always appeared at or after the end of seizure. Because the same characteristic of epileptiform calcium signal appeared in different brain regions, calcium signal may not exist with region specificity, but may exhibit a cell type specific manner. Thus, our work provides a support for the pathogenesis of epilepsy and epileptiform signal transmission research.

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“…In an attempt to identify the extra-hippocampal seizure onset zones in the intraperitoneal KA model of epilepsy, we have examined the electrographic seizure onsets during the acute and pre-SE seizures and later spontaneous recurrent seizures (SRS; Connell et al, 2017). Preceding and simultaneous ictal activity was observed in multiple locations, including the claustrum, which eventually involved the hippocampus (Figure 3).…”

Section: Role Of the Claustrum In Seizuresmentioning

confidence: 99%

“…Claustrum as the seizure onset zone: representative electroencephalography (EEG) indicating the onset of seizure in the right claustrum and propagating to the bilateral hippocampi. From Connell et al (2017)—with permission.…”

Section: Role Of the Claustrum In Seizuresmentioning

confidence: 99%

The Claustrum in Relation to Seizures and Electrical Stimulation

et al. 2019

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The neural mechanisms of altered consciousness that accompanies most epileptic seizures are not known. We have reported alteration of consciousness resulting from electrical stimulation of the claustrum via a depth electrode in a woman with refractory focal epilepsy. Additionally, there are reports that suggest possible claustral involvement in focal epilepsy, including MRI findings of bilaterally increased T2 signal intensity in patients with status epilepticus (SE). Although its cytoarchitecture and connectivity have been studied extensively, the precise role of the claustrum in consciousness processing, and, thus, its contribution to the semiology of dyscognitive seizures are still elusive. To investigate the role of the claustrum in rats, we studied the effect of high-frequency stimulation (HFS) of the claustrum on performance in the operant chamber. We also studied the inter-claustral and the claustro-hippocampal connectivity through cerebro-cerebral evoked potentials (CCEPs), and investigated the involvement of the claustrum in kainate (KA)-induced seizures. We found that HFS of the claustrum decreased the performance in the operant task in a manner that was proportional to the current intensity used. In this article, we present previously unpublished data about the effect of stimulating extra-claustral regions in the operant chamber task as a control experiment. In these animals, stimulation of the corpus callosum, the largest interhemispheric commissure, as well as the orbitofrontal cortex in the vicinity of the claustrum did not produce that same effect as with claustral stimulation. Additionally, CCEPs established the presence of effective connectivity between both claustra, as well as between the claustrum and bilateral hippocampi indicating that these connections may be part of the circuitry involved in alteration of consciousness in limbic seizures. Lastly, some seizures induced by KA injections showed an early involvement of the claustrum with later propagation to the hippocampi. Further work is needed to clarify the exact role of the claustrum in mediating alteration of consciousness during epileptic seizures.

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Acute and spontaneous seizure onset zones in the intraperitoneal kainic acid model

Cited by 14 publications

References 13 publications

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

Stereotypical patterns of epileptiform calcium signal in hippocampal CA1, CA3, dentate gyrus and entorhinal cortex in freely moving mice

The Claustrum in Relation to Seizures and Electrical Stimulation

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