Status Epilepticus Dynamics Predicts Latency to Spontaneous Seizures in the Kainic Acid Model.
Animals
Brain
/ cytology
Cell Death
Cell Survival
/ drug effects
Disease Models, Animal
Electroencephalography
Epilepsy, Temporal Lobe
/ chemically induced
Gamma Rhythm
/ drug effects
Hippocampus
/ cytology
Kainic Acid
Male
Neurons
/ cytology
Rats
Rats, Sprague-Dawley
Seizures
/ pathology
Status Epilepticus
/ chemically induced
Theta Rhythm
/ drug effects
Epileptogenesis; Gamma power; Kainic acid; Status epilepticus; Temporal lobe epilepsy; Theta power
Journal
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN: 1421-9778
Titre abrégé: Cell Physiol Biochem
Pays: Germany
ID NLM: 9113221
Informations de publication
Date de publication:
16 May 2020
16 May 2020
Historique:
accepted:
30
04
2020
entrez:
17
5
2020
pubmed:
18
5
2020
medline:
12
11
2020
Statut:
ppublish
Résumé
Status epilepticus (SE) might be followed by temporal lobe epilepsy (TLE), a common neurologic disorder characterized by spontaneous recurrent seizures (SRSs). However, the relationship between SE and TLE is still incompletely characterized. For this reason, in a model of TLE we evaluated the lesion extent and the onset of SRSs to determine if they were influenced by the SE dynamics. Sixty-two adult male Sprague-Dawley rats were implanted for video-electrocorticographic (v-ECoG) monitoring and intraperitoneally treated with saline or kainic acid (KA, 15 mg/kg) at 8 weeks of age. v-ECoG recordings were obtained during SE, in the following 9 weeks, and assessed by amplitude or power band spectrum. Rats were euthanized 3 or 64 days after SE to evaluate the lesion. SE lasted about 10 h during which the mean duration of convulsive seizures (CSs) increased from 39 s, at 30 min, to 603 s at 4 h. The gamma power peaked 30 min after the SE onset and its peak was correlated (r²=0.13, p=0.042) with the overall SE duration. Subsequently, the gamma power was reduced under the baseline until the end of SE. The theta power increased at approximately 150% of basal levels 3 h after KA injection, but it went back to basal levels with the full development of CSs. Interestingly, the timing of the first SRS in chronic epilepsy was correlated with the latency to develop the first CS with loss of posture during SE (r²=0.60, p<0.001). Additionally, the overall duration of CSs observed during SE was related to the number of damaged brain regions (r²=0.60, p=0.005), but it did not influence the timing of the first SRS in chronic epilepsy. Overall, our results show that the onset of chronic epilepsy is modulated by SE dynamics, whereas brain damage is related to prolonged convulsions in SE.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
Status epilepticus (SE) might be followed by temporal lobe epilepsy (TLE), a common neurologic disorder characterized by spontaneous recurrent seizures (SRSs). However, the relationship between SE and TLE is still incompletely characterized. For this reason, in a model of TLE we evaluated the lesion extent and the onset of SRSs to determine if they were influenced by the SE dynamics.
METHODS
METHODS
Sixty-two adult male Sprague-Dawley rats were implanted for video-electrocorticographic (v-ECoG) monitoring and intraperitoneally treated with saline or kainic acid (KA, 15 mg/kg) at 8 weeks of age. v-ECoG recordings were obtained during SE, in the following 9 weeks, and assessed by amplitude or power band spectrum. Rats were euthanized 3 or 64 days after SE to evaluate the lesion.
RESULTS
RESULTS
SE lasted about 10 h during which the mean duration of convulsive seizures (CSs) increased from 39 s, at 30 min, to 603 s at 4 h. The gamma power peaked 30 min after the SE onset and its peak was correlated (r²=0.13, p=0.042) with the overall SE duration. Subsequently, the gamma power was reduced under the baseline until the end of SE. The theta power increased at approximately 150% of basal levels 3 h after KA injection, but it went back to basal levels with the full development of CSs. Interestingly, the timing of the first SRS in chronic epilepsy was correlated with the latency to develop the first CS with loss of posture during SE (r²=0.60, p<0.001). Additionally, the overall duration of CSs observed during SE was related to the number of damaged brain regions (r²=0.60, p=0.005), but it did not influence the timing of the first SRS in chronic epilepsy.
CONCLUSION
CONCLUSIONS
Overall, our results show that the onset of chronic epilepsy is modulated by SE dynamics, whereas brain damage is related to prolonged convulsions in SE.
Substances chimiques
Kainic Acid
SIV03811UC
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
493-507Subventions
Organisme : Ministry of Health
ID : RF-2011-02350485
Pays : Italy
Organisme : University of Modena and Reggio Emilia
ID : FAR2018
Pays : Italy
Organisme : Fondazione Mariani
ID : R-19-110
Pays : Italy
Organisme : MIUR - Ministry of Education, University and Research
Pays : Italy
Organisme : BPER Banca
Pays : Italy
Informations de copyright
© Copyright by the Author(s). Published by Cell Physiol Biochem Press.
Déclaration de conflit d'intérêts
The authors have no conflicts of interest to declare.