ArticleEBioMedicine2016
Entorhinal Principal Neurons Mediate Brain-stimulation Treatments for Epilepsy.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Article
- Nanophotonic neural probes for in vivo photostimulation, electrophysiology, and microfluidic delivery.Microsystems & nanoengineering · 2026Article
- Triptolide Inhibits Epileptic Seizures by Rescuing the Neuroinflammation-Related GABAergic Dysfunction in Mice.CNS neuroscience & therapeutics · 2025Article
- Invasive Neurostimulation for the Treatment of Epilepsy.Seminars in neurology · 2025Review
- A review of cell-type specific circuit mechanisms underlying epilepsy.Acta epileptologica · 2024Review
- Low-frequency Stimulation at the Subiculum Prevents Extensive Secondary Epileptogenesis in Temporal Lobe Epilepsy.Neuroscience bulletin · 2024Article
- Inflachromene attenuates seizure severity in mouse epilepsy models via inhibiting HMGB1 translocation.Acta pharmacologica Sinica · 2023Article
- Subicular circuit in epilepsy: deconstruct heterogeneity for precise therapeutics.Frontiers in neuroscience · 2023Article
- Optogenetic Low-Frequency Stimulation of Principal Neurons, but Not Parvalbumin-Positive Interneurons, Prevents Generation of Ictal Discharges in Rodent Entorhinal Cortex in an In Vitro 4-Aminopyridine Model.International journal of molecular sciences · 2022Article
- Closed-loop direct control of seizure focus in a rodent model of temporal lobe epilepsy via localized electric fields applied sequentially.Nature communications · 2022Article
- Discrete subicular circuits control generalization of hippocampal seizures.Nature communications · 2022Article
- Paradoxical effects of posterior intralaminar thalamic calretinin neurons on hippocampal seizure via distinct downstream circuits.iScience · 2022Article
- Revealing the Precise Role of Calretinin Neurons in Epilepsy: We Are on the Way.Neuroscience bulletin · 2022Review
- Deep brain stimulation in the medial septum attenuates temporal lobe epilepsy via entrainment of hippocampal theta rhythm.CNS neuroscience & therapeutics · 2021Article
- Article
- Pharmaco-genetic inhibition of pyramidal neurons retards hippocampal kindling-induced epileptogenesis.CNS neuroscience & therapeutics · 2020Article
- Neural mass modeling of slow-fast dynamics of seizure initiation and abortion.PLoS computational biology · 2020Article
- Analysis of brain metabolites by gas chromatography-mass spectrometry reveals the risk-benefit concerns of prednisone in MRL/lpr lupus mice.Inflammopharmacology · 2020Article
- A disinhibitory nigra-parafascicular pathway amplifies seizure in temporal lobe epilepsy.Nature communications · 2020Article
- Limited preventive effect of prednisone on neuropsychiatric symptoms in murine systemic lupus erythematosus.Inflammopharmacology · 2019Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain stimulation is an alternative treatment for epilepsy. However, the neuronal circuits underlying its mechanisms remain obscure. We found that optogenetic activation (1Hz) of entorhinal calcium/calmodulin-dependent protein kinase II α (CaMKIIα)-positive neurons, but not GABAergic neurons, retarded hippocampal epileptogenesis and reduced hippocampal seizure severity, similar to that of entorhinal low-frequency electrical stimulation (LFES). Optogenetic inhibition of entorhinal CaMKIIα-positive neurons blocked the antiepileptic effect of LFES. The channelrhodopsin-2-eYFP labeled entorhinal CaMKIIα-positive neurons primarily targeted the hippocampus, and the activation of these fibers reduced hippocampal seizure severity. By combining extracellular recording and pharmacological methods, we found that activating entorhinal CaMKIIα-positive neurons induced the GABA-mediated inhibition of hippocampal neurons. Optogenetic activation of focal hippocampal GABAergic neurons mimicked this neuronal modulatory effect and reduced hippocampal seizure severity, but the anti-epileptic effect is weaker than that of entorhinal LFES, which may be due to the limited spatial neuronal modulatory effect of focal photo-stimulation. Our results demonstrate a glutamatergic-GABAergic neuronal circuit for LFES treatment of epilepsy, which is mediated by entorhinal principal neurons.
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Registered trials
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