ArticleFrontiers in neurology2023
MiR-324-5p inhibition after intrahippocampal kainic acid-induced
Article in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Fast ripple-delta coupling as an early biomarker for post-traumatic epileptogenesis in repetitive brain injury.Epilepsia open · 2026Article
- Astrocytic Igfbp2 Promotes Spontaneous Seizures in a Mouse Model of Mesial Temporal Lobe Epilepsy.Glia · 2026Article
- How Soon is Soon Enough? Consideration of Timing and Disease Etiology for microRNAs in Epilepsy.Epilepsy currents · 2025Review
- Fast Ripple-Delta Coupling as Early Biomarker for Post-Traumatic Epileptogenesis in Repetitive Brain Injury.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Background: Acquired epilepsies are caused by an initial brain insult that is followed by epileptogenesis and finally the development of spontaneous recurrent seizures. The mechanisms underlying epileptogenesis are not fully understood. MicroRNAs regulate mRNA translation and stability and are frequently implicated in epilepsy. For example, antagonism of a specific microRNA, miR-324-5p, before brain insult and in a model of chronic epilepsy decreases seizure susceptibility and frequency, respectively. Here, we tested whether antagonism of miR-324-5p during epileptogenesis inhibits the development of epilepsy. Methods: We used the intrahippocampal kainic acid (IHpKa) model to initiate epileptogenesis in male wild type C57BL/6 J mice aged 6-8 weeks. Twenty-four hours after IHpKa, we administered a miR-324-5p or scrambled control antagomir intracerebroventricularly and implanted cortical surface electrodes for EEG monitoring. EEG data was collected for 28 days and analyzed for seizure frequency and duration, interictal spike activity, and EEG power. Brains were collected for histological analysis. Results: Histological analysis of brain tissue showed that IHpKa caused characteristic hippocampal damage in most mice regardless of treatment. Antagomir treatment did not affect latency to, frequency, or duration of spontaneous recurrent seizures or interictal spike activity but did alter the temporal development of frequency band-specific EEG power. Conclusion: These results suggest that miR-324-5p inhibition during epileptogenesis induced by
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