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Multi-modal characterization and simulation of human epileptic circuitry.
Buchin, Anatoly; de Frates, Rebecca; Nandi, Anirban; Mann, Rusty; Chong, Peter; Ng, Lindsay; Miller, Jeremy; Hodge, Rebecca; Kalmbach, Brian; Bose, Soumita; Rutishauser, Ueli; McConoughey, Stephen; Lein, Ed; Berg, Jim; Sorensen, Staci; Gwinn, Ryder; Koch, Christof; Ting, Jonathan; Anastassiou, Costas A.
Afiliación
  • Buchin A; Allen Institute for Brain Science, Seattle, WA, USA. Electronic address: anat.buchin@gmail.com.
  • de Frates R; Allen Institute for Brain Science, Seattle, WA, USA.
  • Nandi A; Allen Institute for Brain Science, Seattle, WA, USA.
  • Mann R; Allen Institute for Brain Science, Seattle, WA, USA.
  • Chong P; Allen Institute for Brain Science, Seattle, WA, USA.
  • Ng L; Allen Institute for Brain Science, Seattle, WA, USA.
  • Miller J; Allen Institute for Brain Science, Seattle, WA, USA.
  • Hodge R; Allen Institute for Brain Science, Seattle, WA, USA.
  • Kalmbach B; Allen Institute for Brain Science, Seattle, WA, USA; University of Washington, Seattle, WA, USA.
  • Bose S; Allen Institute for Brain Science, Seattle, WA, USA; CiperHealth, San Francisco, CA, USA.
  • Rutishauser U; Department of Neurosurgery, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Center for Neural Science and Medicine, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
  • McConoughey S; Allen Institute for Brain Science, Seattle, WA, USA.
  • Lein E; Allen Institute for Brain Science, Seattle, WA, USA; University of Washington, Seattle, WA, USA.
  • Berg J; Allen Institute for Brain Science, Seattle, WA, USA.
  • Sorensen S; Allen Institute for Brain Science, Seattle, WA, USA.
  • Gwinn R; Swedish Medical Center, Seattle, WA, USA.
  • Koch C; Allen Institute for Brain Science, Seattle, WA, USA.
  • Ting J; Allen Institute for Brain Science, Seattle, WA, USA; University of Washington, Seattle, WA, USA.
  • Anastassiou CA; Allen Institute for Brain Science, Seattle, WA, USA; Department of Neurosurgery, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center,
Cell Rep ; 41(13): 111873, 2022 12 27.
Article en En | MEDLINE | ID: mdl-36577383
Temporal lobe epilepsy is the fourth most common neurological disorder, with about 40% of patients not responding to pharmacological treatment. Increased cellular loss is linked to disease severity and pathological phenotypes such as heightened seizure propensity. While the hippocampus is the target of therapeutic interventions, the impact of the disease at the cellular level remains unclear. Here, we show that hippocampal granule cells change with disease progression as measured in living, resected hippocampal tissue excised from patients with epilepsy. We show that granule cells increase excitability and shorten response latency while also enlarging in cellular volume and spine density. Single-nucleus RNA sequencing combined with simulations ascribes the changes to three conductances: BK, Cav2.2, and Kir2.1. In a network model, we show that these changes related to disease progression bring the circuit into a more excitable state, while reversing them produces a less excitable, "early-disease-like" state.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Epilepsia / Epilepsia del Lóbulo Temporal Límite: Humans Idioma: En Revista: Cell Rep Año: 2022 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Epilepsia / Epilepsia del Lóbulo Temporal Límite: Humans Idioma: En Revista: Cell Rep Año: 2022 Tipo del documento: Article Pais de publicación: Estados Unidos