Seizures in the intrahippocampal kainic acid epilepsy model: characterization using long-term video-EEG monitoring in the rat

Raedt, Robrecht; Dycke, Annelies Van; Melkebeke, Deborah Van; Smedt, Tim De; Claeys, Pieter W.; Wyckhuys, Tine; Vonck, Kristl; Wadman, Wytse J.; Boon, Paul

doi:10.1111/j.1600-0404.2008.01108.x

Cited by 86 publications

(80 citation statements)

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“…In comparison to the repeated low dose KA-injection protocol, systemic pilocarpine induced SE has a higher mortality rate of 30-50% (Curia et al, 2008), and mortality rate in the stimulation SE models is comparable with our observations. All rats we injected with KA developed a self-sustained SE consistent with reports on the intrahippocampal KA model (Raedt et al, 2009). Despite injection issues, about 83% of the rats develop SE in the ip.…”

Section: Discussionsupporting

confidence: 74%

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

et al. 2015

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Section: Discussionsupporting

confidence: 74%

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

et al. 2015

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“…Intrahippocampal KA delivery in the current study produced recurrent seizure activity lasting for several hours, similar to previous studies (56). This seizure activity was associated with an early activation of the sympathetic system, as demonstrated by increased plasma noradrenaline levels, tachycardia, and elevated BP within 3 h. The sympathovagal balance changed in favor of sympathetic dominance at 48 h and 7 days following seizure induction.…”

Section: Discussionsupporting

confidence: 65%

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus

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Millen

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Seizures are associated with altered autonomic activity, which has been implicated in the development of cardiac dysfunction and structural damage. This study aimed to investigate the involvement of the autonomic nervous system in seizure-induced cardiomyopathy. Male Sprague-Dawley rats (320 -350 g) were implanted with EEG/ECG electrodes to allow simultaneous telemetric recordings during seizures induced by intrahippocampal (2 nmol, 1 l/min) kainic acid and monitored for 7 days. Seizure activity occurred in conjunction with increased heart rate (20%), blood pressure (25%), and QTc prolongation (15%). This increased sympathetic activity was confirmed by the presence of raised plasma noradrenaline levels at 3 h post-seizure induction. By 48 h post-seizure induction, sympathovagal balance was shifted in favor of sympathetic dominance, as indicated by both heart rate variability (LF/HF ratio of 3.5 Ϯ 1.0) and pharmacological autonomic blockade. Functional cardiac deficits were evident at 7 and 28 days, as demonstrated by echocardiography showing a decreased ejection fraction (14% compared with control, P Ͻ 0.05) and dilated cardiomyopathy present at 28 days following seizure induction. Histological changes, including cardiomyocyte vacuolization, cardiac fibrosis, and inflammatory cell infiltration, were evident within 48 h of seizure induction and remained present for up to 28 days. These structural changes most probably contributed to an increased susceptibility to aconitine-induced arrhythmias. This study confirms that prolonged seizure activity results in acute and chronic alterations in cardiovascular control, leading to a deterioration in cardiac structure and function. This study further supports the need for modulation of sympathetic activity as a promising therapeutic approach in seizure-induced cardiomyopathy.

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“…The most interesting compounds identified by the protocol described above will be tested in at least one other post-SE model of TLE [i.e., SE induced by sustained BLA stimulation (Brandt et al, 2003a) or intrahippocampal administration of kainate (Raedt et al, 2009)]. In both models, the SE and its consequences are less severe compared with systemic administration of pilocarpine (Brandt et al, 2003a;Dudek et al, 2006), thus enhancing the chance of identifying potentially useful antiepileptogenic therapies.…”

Section: Antiepileptogenesis After Brain Insultsmentioning

confidence: 99%

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

Löscher¹,

Brandt²

2010

Pharmacol Rev

364

366

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Seizures in the intrahippocampal kainic acid epilepsy model: characterization using long-term video-EEG monitoring in the rat

Abstract: This study shows that the characteristics of spontaneous seizures in the intrahippocampal KA model display many similarities to other SE models and human temporal lobe epilepsy.

Cited by 86 publications

References 58 publications

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

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

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus

Prevention or Modification of Epileptogenesis after Brain Insults: Experimental Approaches and Translational Research

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