Targeted Augmentation of Nuclear Gene Output (TANGO) of Scn1a rescues parvalbumin interneuron excitability and reduces seizures in a mouse model of Dravet Syndrome
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Title
Targeted Augmentation of Nuclear Gene Output (TANGO) of Scn1a rescues parvalbumin interneuron excitability and reduces seizures in a mouse model of Dravet Syndrome
Authors
Keywords
Epilepsy, Antisense oligonucleotide (ASO), Voltage-gated sodium channel, Parvalbumin-positive (PV) inhibitory interneuron, STK-001
Journal
BRAIN RESEARCH
Volume 1775, Issue -, Pages 147743
Publisher
Elsevier BV
Online
2021-11-27
DOI
10.1016/j.brainres.2021.147743
References
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Note: Only part of the references are listed.- Scn8a Antisense Oligonucleotide Is Protective in Mouse Models of SCN8A Encephalopathy and Dravet Syndrome
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- Antisense oligonucleotide modulation of non-productive alternative splicing upregulates gene expression
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- Antisense oligonucleotides increase Scn1a expression and reduce seizures and SUDEP incidence in a mouse model of Dravet syndrome
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- Vasoactive intestinal peptide-expressing interneurons are impaired in a mouse model of Dravet syndrome
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- Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome
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- Diagnosis and long-term course of Dravet syndrome
- (2012) Ingrid E. Scheffer EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY
- Preferential inactivation of Scn1a in parvalbumin interneurons increases seizure susceptibility
- (2012) Stacey B. Dutton et al. NEUROBIOLOGY OF DISEASE
- Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome
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- The core Dravet syndrome phenotype
- (2011) Charlotte Dravet EPILEPSIA
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