Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy

By Frank H Yu, M. Mantegazza, G. S. McKnight, T. Scheuer, Judit K. Makara, M. Mor, D. Fegley, S. I. Szabó, S. Kathuria, G. Astarita and 5 more. Nature Neuroscience, 2006

998 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/3350471bacbc5ac58b0b5f9a486379216cd20aac

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Maarten H. P. Kole
2. G. Stuart
3. Takao K. Hensch
4. Frank Sengpiel
5. Bart Larsen
6. D. Feldman
7. Janet F. Werker
8. Beatriz Luna

In Molecular Biology

1. Mark Gerstein
2. Maarten H. P. Kole
3. G. Stuart
4. Takao K. Hensch
5. Frank Sengpiel
6. D. Feldman
7. Bart Larsen
8. Beatriz Luna

In Psychiatry and Mental health

1. Takao K. Hensch

Citations in the corpus

• FOXG1-dependent dysregulation of GABA/glutamate neuron differentiation in autism spectrum disorders (2015, positive): “This isoform is preferentially expressed in GABAergic interneurons (Cheah et al., 2012; Han et al., 2012; Ogiwara et al., 2007; Yu et al., 2006) and the increased proportion of cells with this sodium channel phenotype is consistent with a greater proportion of GABAergic neurons in cortical…”
• Nav1.1 Localizes to Axons of Parvalbumin-Positive Inhibitory Interneurons: A Circuit Basis for Epileptic Seizures in Mice Carrying an Scn1a Gene Mutation (2007, background): “Recently, Yu et al. (2006) generated Nav1.”
• Signal processing in the axon initial segment. (2012, positive): “1 knockout mice showed increased spike frequency adaptation, consistent with reduced somatic whole-cell Na+ current (Ogiwara et al., 2007; Yu et al., 2006).”
• Seizures and epilepsy: an overview for neuroscientists. (2015, background): “The cellular defect may be abnormal sodium channels in cortical interneurons, allowing increased firing of downstream excitatory pyramidal neurons, which are released from inhibitory control (Yu et al. 2006).”