A5015381057- Neuroscience and Neuropharmacology Research
- Ion channel regulation and function
- Epilepsy research and treatment
- Marine Toxins and Detection Methods
- Nicotinic Acetylcholine Receptors Study
- Chemical synthesis and alkaloids
- Treatment of Major Depression
- Pain Management and Placebo Effect
- Marine Sponges and Natural Products
- Psychedelics and Drug Studies
- Neural dynamics and brain function
- Advanced Memory and Neural Computing
- Retinal Development and Disorders
- Neuroscience and Neural Engineering
- Anesthesia and Sedative Agents
- RNA regulation and disease
Stanford Medicine
2024
University of Michigan
2018-2023
Abstract Dravet syndrome is an intractable developmental and epileptic encephalopathy caused by de novo variants in SCN1A resulting haploinsufficiency of the voltage-gated sodium channel Nav1.1. We showed previously that administration antisense oligonucleotide STK-001, also called ASO-22, generated using targeted augmentation nuclear gene output technology to prevent inclusion nonsense-mediated decay, or poison, exon 20N human SCN1A, increased productive Scn1a transcript Nav1.1 expression...
Small molecules that bind to voltage-gated sodium channels (VGSCs) are promising leads in the treatment of numerous neurodegenerative diseases and pain. Nature is a highly skilled medicinal chemist this regard, designing potent VGSC ligands capable binding blocking channel, thereby offering compounds potential therapeutic interest. Paralytic shellfish toxins (PSTs), produced by cyanobacteria marine dinoflagellates, examples these naturally occurring small molecule blockers can potentially be...
Human variants in voltage-gated sodium channel (VGSC) α and β subunit genes are linked to developmental epileptic encephalopathies (DEEs). Inherited, biallelic, loss-of-function SCN1B, encoding the β1/β1B subunits, early infantile DEE (EIEE52). De novo, monoallelic SCN1A (Nav1.1), SCN2A (Nav1.2), SCN3A (Nav1.3), SCN8A (Nav1.6) also DEEs. While these VGSC-linked DEEs have similar presentations, they diverse mechanisms of altered neuronal excitability. Mouse models suggested that Scn2a-,...
Abstract Voltage gated sodium channels (VGSCs) are required for action potential initiation and propagation in mammalian neurons. As with other ion channel families, VGSC density varies between Importantly, current ( I Na ) variability is reduced pyramidal neurons of Scn1b null mice . encodes the β1/ β1B subunits, which regulate expression, trafficking, voltage dependent properties. Here, we investigate how variable cortical layer 6 subicular affects spike patterning network synchronization....