Kevin J. Bender

The paper shows that Scn2a loss-of-function in mice causes degraded sensory coding in the cortex, which is rescued by CRISPRa gene activation.

This study shows that Scn2a haploinsufficiency impairs dendritic signaling and flexible decision-making in mice.

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 investigates the distinct roles of NaV1.2 and NaV1.6 in neocortical pyramidal cell excitability using inhibitors and genetic modifications to selectively block each isoform.

This study identifies D3R-expressing neurons in the NAc as mediators of quetiapine's aversive effects, showing that chronic treatment reduces this aversion.

This paper introduces opto-δL, a method to identify and quantify electrical synapses, and applies it to map coupled networks in thalamic and cortical tissues.

This study investigates how delta opioid receptors modulate GABA release in prefrontal interneurons through distinct signaling pathways, affecting synaptic inhibition in somatic and dendritic compartments.

This study shows that group 2 innate lymphoid cells (ILC2s) and their cytokine IL-13 promote inhibitory synapse development and adult social behavior.

The paper identifies impaired cerebellar plasticity as a mechanism underlying hypersensitized sensory reflexes in SCN2A-associated ASD, showing that increasing Scn2a expression rescues VOR plasticity in mice.

This study shows that Ank2 and Scn2a work together in dendrites of neocortical neurons, linking their dysfunction to autism spectrum disorder.

This study shows that GABA at the axon initial segment inhibits action potential initiation in prefrontal cortex neurons across periadolescent development.

This study identifies some second generation antipsychotics (SGAs) as arrestin-3 agonists at D3 dopamine receptors, showing that chronic use leads to receptor degradation and altered drug efficacy.

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.

This paper investigates the effects of the SCN2A p.K1422E variant in mice, showing mixed functional and behavioral impacts on neurons and neurodevelopmental phenotypes.

NeuroGPU accelerates biophysically detailed neuronal simulations on GPUs, enabling faster parameter exploration and model fitting.

The paper quantifies developmental changes in voltage-gated sodium channel exon expression in human and mouse neocortex, identifying key splicing transitions associated with neurological disorders.

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 paper uses CNNs to infer neuronal ionic conductances from simulated membrane potentials, achieving better accuracy than traditional optimization methods.

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.

The paper generates and validates two knock-in rat strains expressing Cre or Flp recombinase under the Parvalbumin promoter for studying inhibitory interneurons.