Nouveau modèle animal d’épilepsie temporale

Carmant, Lionel

doi:10.1051/medsci/20072311929

Cited by 6 publications

(5 citation statements)

References 16 publications

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“…over 60 minutes), SRS are much more longer and severe although occurring only in a similar proportion of animals [34]. At odds with these earlier studies, we did not observe SRS during the prolonged video-EEG monitoring of unlesioned male rats following hyperthermic seizures [2], [4], [5], [7], [20], [33]. Whereas seizure duration is approximately the same in both protocols, it should be noted that the exposure to hyperthermia was shorter in our experiment, this could explain the observed differences in outcomes [9].…”

Section: Discussioncontrasting

confidence: 70%

“…The rationale of the model is that the presence of a cortical malformation induced at P1, leads to enhanced susceptibility to a second insult, the hyperthermic seizure (HS) at P10. Indeed, control pups not exposed to the initial insult only experience brief HS and do not develop spontaneous recurrent seizures (SRS), while all lesioned pups exposed to hyperthermia for a similar period of time develop febrile status epilepticus (LHS pups) followed by MTLE after a latent period of approximately 80 days [2], [4], [5], [7]. In comparison, other models of prolonged HS in naïve animals produced by prolonged exposure to high temperature lead to chronic epilepsy in about a third of pups [8], [9], while the rats exposed to the freeze lesion alone do not experience SRS [4].…”

Section: Introductionmentioning

confidence: 99%

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Early-Life Stress Is Associated with Gender-Based Vulnerability to Epileptogenesis in Rat Pups

et al. 2012

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During development, the risk of developing mesial temporal lobe epilepsy (MTLE) increases when the developing brain is exposed to more than one insult in early life. Early life insults include abnormalities of cortical development, hypoxic-ischemic injury and prolonged febrile seizures. To study epileptogenesis, we have developed a two-hit model of MTLE characterized by two early-life insults: a freeze lesion-induced cortical malformation at post-natal day 1 (P1), and a prolonged hyperthermic seizure (HS) at P10. As early life stressors lead to sexual dimorphism in both acute response and long-term outcome, we hypothesized that our model could lead to gender-based differences in acute stress response and long-term risk of developing MTLE. Male and female pups underwent a freeze-lesion induced cortical microgyrus at P1 and were exposed to HS at P10. Animals were monitored by video-EEG from P90 to P120. Pre and post-procedure plasma corticosterone levels were used to measure stress response at P1 and P10. To confirm the role of sex steroids, androgenized female pups received daily testosterone injections to the mother pre-natally and post-natally for nine days while undergoing both insults. We demonstrated that after both insults females did not develop MTLE while all males did. This correlated with a rise in corticosterone levels at P1 following the lesion in males only. Interestingly, all androgenized females showed a similar rise in corticosterone at P1, and also developed MTLE. Moreover, we found that the cortical lesion significantly decreased the latency to generalized convulsion during hyperthermia at P10 in both genders. The cortical dysplasia volumes at adulthood were also similar between male and female individuals. Our data demonstrate sexual dimorphism in long-term vulnerability to develop epilepsy in the lesion + hyperthermia animal model of MTLE and suggest that the response to early-life stress at P1 contributes significantly to epileptogenesis in a gender-specific manner.

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Section: Discussioncontrasting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Early-Life Stress Is Associated with Gender-Based Vulnerability to Epileptogenesis in Rat Pups

et al. 2012

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“…All hyperthermia-treated rats developed rapidly generalised seizures. This result is consistent with previous data suggesting that, in the immature healthy brain, a high and prolonged temperature is required for convulsive seizures to appear [ 27 ].…”

Section: Discussionsupporting

confidence: 93%

Hyperthermia-Induced Febrile Seizures Have Moderate and Transient Effects on Spatial Learning in Immature Rats

Yagoubi¹,

Jomni²,

Sakly³

2015

Behavioural Neurology

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The aim of this study was to characterize a novel animal model hyperthermia-induced febrile seizure and to investigate the impacts of repetitive febrile seizures on spatial learning and memory performances in immature rats. Methods. Rats were subjected to hyperthermia exposure one, two, or three times in 10-day intervals during 30 min in a water bath warmed at 45–50°C and their behaviour was monitored. Morris water maze spatial learning and memory were examined for control and treated groups. Results showed that rats subjected to 30-minute hyperthermia hot water developed rapidly myoclonic jerks and then generalized seizures. After a single hyperthermia exposure, the time for generalised tonic-clonic seizures appearance was 16.08 ± 0.60 min and it decreased gradually with repetitive exposure to reach 12.46 ± 0.39 min by the third exposure. Febrile seizures altered the spatial learning and memory abilities in Morris water maze and increased the time spent to attain the platform after one or two exposures, while after a third exposure rats exhibited the same latency compared to controls. Similar results were obtained in probe test where rats, subjected to hyperthermia for one or two episodes, spent less time in the target quadrant compared to corresponding controls. Further, when platform was moved from northwest to southwest quadrant, memory transfer test indicated that after one or two hyperthermia exposures cognitive performances were slightly altered, while after a third exposure the latency to escape increased significantly compared to untreated group. It was concluded that 30 min of hyperthermia hot water was sufficient to induce febrile seizures in immature rats and an increase of susceptibility was observed with repetitive hyperthermia exposure. Hyperthermia treatment impaired cognitive performances but the effects were mostly transient and moderate.

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“…Often, no HS or only mild forms of it (noHS) occur in sKA and sPilo models (Okazaki et al, 1999; Scharfman et al, 2000; Dietrich et al, 2005; Curia et al, 2014). In contrast, development of HS and GCD, as well as focal spontaneous TLE seizures, can be induced by intracranial (intrahippocampal) kainate injection (iKA) (Suzuki et al, 1995; Fritschy, 2004). Another TLE model, which reproduces HS and chronic (bilateral) seizures, is perforant path stimulation-induced non-convulsive- (Kienzler et al, 2009) or convulsive SE (Bumanglag and Sloviter, 2008).…”

Section: Temporal Lobe Epilepsymentioning

confidence: 99%

Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential

Wolfart

Laker

2015

Front. Physiol.

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Neurons continuously adapt the expression and functionality of their ion channels. For example, exposed to chronic excitotoxicity, neurons homeostatically downscale their intrinsic excitability. In contrast, the “acquired channelopathy” hypothesis suggests that proepileptic channel characteristics develop during epilepsy. We review cell type-specific channel alterations under different epileptic conditions and discuss the potential of channels that undergo homeostatic adaptations, as targets for antiepileptic drugs (AEDs). Most of the relevant studies have been performed on temporal lobe epilepsy (TLE), a widespread AED-refractory, focal epilepsy. The TLE patients, who undergo epilepsy surgery, frequently display hippocampal sclerosis (HS), which is associated with degeneration of cornu ammonis subfield 1 pyramidal cells (CA1 PCs). Although the resected human tissue offers insights, controlled data largely stem from animal models simulating different aspects of TLE and other epilepsies. Most of the cell type-specific information is available for CA1 PCs and dentate gyrus granule cells (DG GCs). Between these two cell types, a dichotomy can be observed: while DG GCs acquire properties decreasing the intrinsic excitability (in TLE models and patients with HS), CA1 PCs develop channel characteristics increasing intrinsic excitability (in TLE models without HS only). However, thorough examination of data on these and other cell types reveals the coexistence of protective and permissive intrinsic plasticity within neurons. These mechanisms appear differentially regulated, depending on the cell type and seizure condition. Interestingly, the same channel molecules that are upregulated in DG GCs during HS-related TLE, appear as promising targets for future AEDs and gene therapies. Hence, GCs provide an example of homeostatic ion channel adaptation which can serve as a primer when designing novel anti-epileptic strategies.

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Nouveau modèle animal d’épilepsie temporale

Cited by 6 publications

References 16 publications

Early-Life Stress Is Associated with Gender-Based Vulnerability to Epileptogenesis in Rat Pups

Early-Life Stress Is Associated with Gender-Based Vulnerability to Epileptogenesis in Rat Pups

Hyperthermia-Induced Febrile Seizures Have Moderate and Transient Effects on Spatial Learning in Immature Rats

Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential

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