On the Origin of Interictal Activity in Human Temporal Lobe Epilepsy in Vitro

By I. Cohen, V. Navarro, S. Clemenceau, M. Baulac, R. Miles. Science, 2002

1,011 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8e3c0567d8ee85d80760eb3deeae0907e11239db

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

In Molecular Biology

Citations in the corpus

NKCC1 transporter facilitates seizures in the developing brain (2005, background): “It has recently been shown that subicular neurons from individuals with intractable seizures accumulate Cl − such that GABA A -R activation is excitator”
Drug Resistance in Epilepsy: Clinical Impact, Potential Mechanisms, and New Innovative Treatment Options (2020, background): “Upregulation of NKCC1 and downregulation of KCC2 in the hippocampus have been described both in patients with TLE and the kindling and pilocarpinemodels of TLE (Löscher et al., 2013b).”
Epileptic seizure prediction and control (2003, background): “neuronal network level is one critical factor for epileptogenesis [22]–[26].”
Perturbed Chloride Homeostasis and GABAergic Signaling in Human Temporal Lobe Epilepsy (2007, background): “In patients with temporal lobe epilepsies, depolarizing GABAergic events in a minority of subicular pyramidal cells (Cohen et al., 2002) contribute to interictal-like activity generated in the subiculum.”
Hippocampal sharp wave‐ripple: A cognitive biomarker for episodic memory and planning (2015, background): “While p-ripples induced by blockade of GABAA receptors may form a specific group, studies of ex-in vivo tissue from patients with pharmacoresistant epilepsy paint a more complex picture (Cohen et al., 2002; Alvarado-Rojas et al., 2015).”
Cation-chloride cotransporters and neuronal function. (2009, background): “…study, Miles and coworkers showed that hippocampal slices obtained from temporal lobe epilepsy patients generated interictal activity that was attributable to depolarizing GABA A -mediated transmission in a subpopulation of principal neurons (Cohen et al., 2002; see also Kohling et al., 1998).”