ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Hyperexcitability, interneurons, and loss of GABAergic synapses in entorhinal cortex in a model of temporal lobe epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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92 citing papers in PubMed, 181 citations in OpenAlex.
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- Distinct Transcriptional States of TDP-43 Pathology in an Alzheimer's Disease Mouse Model.Neuroscience bulletin · 2026Article
- Unique deficits in place coding across subfields of the hippocampus in a mouse model of temporal lobe epilepsy.Epilepsia · 2026Article
- Updated Neuronal Numbers of the Rat Hippocampal Formation: Redesigning the Hippocampal Model.Hippocampus · 2026Article
- UNIQUE DEFICITS IN PLACE CODING ACROSS SUBFIELDS OF THE HIPPOCAMPUS IN A MOUSE MODEL OF TEMPORAL LOBE EPILEPSY.bioRxiv : the preprint server for biology · 2025Article
- Ferroptosis-associated transcriptional factors in neurological diseases: molecular mechanisms and therapeutic prospects.Experimental & molecular medicine · 2025Review
- Upregulation of CCK3R leading to the suppression of chronic seizures.Translational psychiatry · 2025Article
- Virtual brain twins for stimulation in epilepsy.Nature computational science · 2025Article
- Article
- Distinct changes to hippocampal and medial entorhinal circuits emerge across the progression of cognitive deficits in epilepsy.Cell reports · 2025Article
- Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathy.JCI insight · 2024Article
- Comparative analysis of hippocampal extracellular space uncovers widely altered peptidome upon epileptic seizure in urethane-anaesthetized rats.Fluids and barriers of the CNS · 2024Article
- The sulfonadyns: a class of aryl sulfonamides inhibiting dynamin I GTPase and clathrin mediated endocytosis are anti-seizure in animal models.RSC medicinal chemistry · 2023Article
- Cell therapy for neurological disorders: Progress towards an embryonic medial ganglionic eminence progenitor-based treatment.Frontiers in neuroscience · 2023Review
- Antidepressant Drugs for Seizures and Epilepsy: Where do we Stand?Current neuropharmacology · 2023Review
- Functional Neurophysiological Biomarkers of Early-Stage Alzheimer's Disease: A Perspective of Network Hyperexcitability in Disease Progression.Journal of Alzheimer's disease : JAD · 2022Review
- Somatostatin-Positive Interneurons Contribute to Seizures inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- PHF24 is expressed in the inhibitory interneurons in rats.Experimental animals · 2021Article
- d-Serine Intervention In The Medial Entorhinal Area Alters TLE-Related Pathology In CA1 Hippocampus Via The Temporoammonic Pathway.Neuroscience · 2021Article
- 3D Ultrastructural Study of Synapses in the Human Entorhinal Cortex.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
32 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
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Abstract
Temporal lobe epilepsy is the most common type of epilepsy in adults, and its pathophysiology remains unclear. Layer II stellate cells of the entorhinal cortex, which are hyperexcitable in animal models of temporal lobe epilepsy, provide the predominant synaptic input to the hippocampal dentate gyrus. Previous studies have ascribed the hyperexcitability of layer II stellate cells to GABAergic interneurons becoming "dormant" after disconnection from their excitatory synaptic inputs, which has been reported to occur during preferential loss of layer III pyramidal cells. We used whole-cell recording from slices of entorhinal cortex in pilocarpine-treated epileptic rats to test the dormant interneuron hypothesis. Hyperexcitability appeared as multiple action potentials and prolonged depolarizations evoked in layer II stellate cells of epileptic rats but not controls. However, blockade of glutamatergic synaptic transmission caused similar percentage reductions in the frequency of spontaneous IPSCs in layer II stellate cells of control and epileptic rats, suggesting similar levels of excitatory synaptic input to GABAergic interneurons. Direct recordings and biocytin labeling revealed two major types of interneurons in layer III whose excitatory synaptic drive in epileptic animals was undiminished. Interneurons in layer III did not appear to be dormant; therefore, we tested whether loss of GABAergic synapses might underlie hyperexcitability of layer II stellate cells. Stereological evidence of fewer GABAergic interneurons, fewer gephyrin-immunoreactive punctae, and reduced frequency of spontaneous IPSCs and miniature IPSCs (recorded in tetrodotoxin) confirmed that layer II stellate cell hyperexcitability is attributable, at least in part, to reduced inhibitory synaptic input.
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