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Published on: June 29, 2022
Does angiogenesis play a role in the establishment of mesial temporal lobe epilepsy?
Ruba Benini1, Raquel Roth2, Zehra Khoja2
1Division of Pediatric Neurology, Department of Pediatrics, Montreal Children's Hospital, Canada.
Abstract:
Mesial temporal lobe epilepsy (MTLE) is a focal epileptic disorder that is frequently associated with hippocampal sclerosis. This study investigated whether blocking angiogenesis prevents the development of seizures and hippocampal atrophy in the pilocarpine rat model of MTLE. To block angiogenesis, a subset of animals were given sunitinib orally. Continuous video recordings were performed to identify seizures. Brains were then extracted and sectioned, and hippocampal surfaces and angiogenesis were assessed. After a latent period of 6.6 ± 2.6 days, the sham-treated pilocarpine rats presented convulsive seizures, while the pilocarpine rats treated with sunitinib did not develop seizures. Sham-treated pilocarpine rats but not sunitinib-treated pilocarpine rats had significantly smaller hippocampi. Endothelial cell counts in sham-treated pilocarpine rats were significantly greater than in controls and sunitinib-treated pilocarpine rats. Blocking angiogenesis immediately following the initial insult in this animal model prevented thus angiogenesis and hippocampal atrophy and averted the development of clinical seizures.
Insights
Blocking angiogenesis prevents seizures and hippocampal atrophy in a rat model of mesial temporal lobe epilepsy (MTLE). This finding suggests anti-angiogenesis therapies could treat epilepsy.
Area of Science:
- Neuroscience
- Epileptology
- Vascular Biology
Background:
- Mesial temporal lobe epilepsy (MTLE) is a common focal epilepsy often linked to hippocampal sclerosis.
- Angiogenesis, the formation of new blood vessels, is implicated in epilepsy development.
Purpose of the Study:
- To investigate if blocking angiogenesis prevents seizures and hippocampal atrophy in the pilocarpine rat model of MTLE.
- To assess the role of angiogenesis in the development of epilepsy-associated brain damage.
Main Methods:
- Rats were treated with sunitinib, an angiogenesis inhibitor, or a sham treatment after pilocarpine-induced insult.
- Continuous video monitoring identified seizure development.
- Histological analysis assessed hippocampal atrophy and angiogenesis (endothelial cell counts).
Main Results:
- Sunitinib-treated rats did not develop seizures, unlike sham-treated rats.
- Sham-treated rats showed significant hippocampal atrophy and increased endothelial cell counts.
- Sunitinib treatment prevented both seizures and hippocampal atrophy, with reduced endothelial cell counts.
Conclusions:
- Blocking angiogenesis immediately after the initial insult prevents the development of clinical seizures in the pilocarpine rat model.
- Inhibition of angiogenesis effectively prevents subsequent hippocampal atrophy and seizure development in MTLE.
- Targeting angiogenesis represents a potential therapeutic strategy for treating MTLE.
