Epileptogenesis and neuropathology after different types of status epilepticus induced by prolonged electrical stimulation of the basolateral amygdala in rats

Brandt, Claudia; Glien, Maike; Potschka, Heidrun; Volk, Holger A.; Löscher, Wolfgang

doi:10.1016/s0920-1211(03)00114-1

Cited by 129 publications

(147 citation statements)

References 34 publications

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“…Commonly, the systemic or intracerebral injections of chemical convulsants such as pilocarpine or kainic acid have been used (Ben-Ari et al, 1980;Cavalheiro et al, 1982;Turski et al, 1983). Also, prolonged stimulation of the hippocampus and other limbic regions with implanted electrodes has been used to produce self-sustaining SE (McIntyre et al, 1982;Brandt et al, 2003). With each protocol, animals acutely demonstrate behavioral and electrographic activity consistent with clinical SE and, if allowed to continue for a sufficient duration, develop some hippocampal neuronal damage that is also observed in humans.…”

Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

254

285

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

254

285

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“…First, although a SE duration of 60 to 90 min is sufficient to induce epilepsy in the majority of rats or mice with systemic administration of pilocarpine or kainate, 3 to 4 h of SE are needed in this respect in models in which SE is induced by focal electrical stimulation of amygdala or hippocampus (Brandt et al, 2003a;Pitkä nen et al, 2005;Mazarati et al, 2006b). Chemically induced SE is more severe than SE induced by electrical stimulation and more difficult to terminate by AEDs such as diazepam (Bankstahl and Löscher, 2008).…”

Section: Antiepileptogenesis After Brain Insultsmentioning

confidence: 99%

“…However, all except one of the MK-801-treated rats developed SRS. Data were reanalyzed from the study of Brandt et al (2003a). In B, SE was induced by sustained electrical stimulation of the BLA.…”

Section: Novel Approaches For Antiepileptogenesis In Post-status Epilmentioning

confidence: 99%

“…Only a few studies examined potential interstrain and intergender differences when the same protocol for SE induction was used, but overall results from different studies have not shown major differences in the development of behavioral and electrographic alterations (Curia et al, 2008). We directly compared the characteristics and long-term consequences of SE induced by sustained stimulation of the BLA in male and female Wistar and Sprague-Dawley rats (Brandt et al, 2003a). Female Sprague-Dawley rats were most sensitive to BLA stimulation in terms of SE induction and development of epilepsy after SE, so that we used this strain and gender for all subsequent experiments.…”

Section: Antiepileptogenesis After Brain Insultsmentioning

confidence: 99%

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

Löscher¹,

Brandt²

2010

Pharmacol Rev

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346

354

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“…In a similar model of SSSE after electrical stimulation of limbic afferents, distinct behavioral types of SSSE were observed as well (29). Interestingly, in that study, neuronal damage, which was not assessed currently, was much more severe in rats with continuous GCSE compared with rats with nonconvulsive partial SE.…”

Section: Discussionmentioning

confidence: 70%

Limbic Self‐sustaining Status Epilepticus in Rats Is Not Associated with Hyperthermia

et al. 2005

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Summary: Purpose:To evaluate the impact of limbic status epilepticus on temperature.Methods: The perforant path in freely moving rats was stimulated electrically for 120 min to induce self-sustaining status epilepticus (SSSE). For 150 min after the end of stimulation, epidural temperature and electrographic and clinical seizure activity were assessed in animals with limbic and motor SSSE, as well as in animals without development of SE.Results: Temperature in all animals with SSSE was elevated by 1.5 ± 0.8• C after the end of stimulation compared with baseline values (p < 0.01). In animals with pure limbic SE, temperature decreased continuously to baseline values over the 150-min period of observation. In contrast, in animals with motor SSSE, temperature remained elevated during continuing epileptic activity and was still significantly higher 150 min after the end of stimulation compared with baseline (p < 0.01). In animals that did not develop SSSE, temperature was not changed after the end of electrical stimulation and in the 150 min thereafter compared with baseline values. Conclusions:The results indicate that hyperthermia as seen in SE is the consequence of motor convulsions and not of epileptic activity itself, as seen in limbic SSSE.

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Epileptogenesis and neuropathology after different types of status epilepticus induced by prolonged electrical stimulation of the basolateral amygdala in rats

Cited by 129 publications

References 34 publications

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

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

Limbic Self‐sustaining Status Epilepticus in Rats Is Not Associated with Hyperthermia

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