Perry W.E. Spratt

This study uses CRISPR activation to upregulate SCN1A in PV interneurons, improving survival and reducing seizures in Dravet syndrome models.

This study shows that CRISPR activation can rescue electrophysiological deficits in SCN2A haploinsufficiency by increasing the expression of the remaining functional allele in mice and human neurons.

This study uses calcium imaging and optical DBS in parkinsonian mice to show that STN DBS disrupts STN activity dynamics, not inhibition or antidromic activation, to relieve motor symptoms.

The paper shows that loss of NaV1.2 sodium channels in pyramidal neurons leads to hyperexcitability and seizures despite reduced action potential size and speed.

The paper investigates calcium channel distribution in the axon initial segment of mouse neurons and finds distinct functional roles for CaV2 and CaV3 channels.

This study shows that the autism-associated gene Scn2a is critical for synaptic stability and learning by regulating dendritic excitability and synaptic function in neurons.