Richard C. Johnson

This study identifies a gain-of-function mutation in GRIA1 causing neurodevelopmental deficits and shows that an antisense oligonucleotide can prevent pathology and behavioral issues.

This paper demonstrates that CRISPR-mediated transcriptional activation can upregulate SYNGAP1 in a mouse model of SRID and human neurons, rescuing deficits without targeting mutations.

This study shows that calcium-permeable AMPA receptors (CP-AMPARs) in PV interneurons reduce their feature selectivity, and removing them increases selectivity in visual cortex and hippocampus.

This study shows WWC2 regulates GABAAR trafficking at inhibitory synapses, distinct from its homolog KIBRA's role at excitatory synapses.

This paper generates two knock-in mouse models with human SYNGAP1 mutations causing intellectual disability, showing reduced protein levels and recapitulating key disease features.

This study shows SynGAP regulates synaptic plasticity and cognition through phase separation, not its catalytic activity.

This study identifies Btbd11 as an inhibitory interneuron-specific protein that supports glutamatergic synapse structure and function, with implications for neural circuitry and behavior.

This study identifies the KIBRA-PKCγ signaling pathway as crucial for modulating memory performance in both mice and humans.

The paper develops tools to track synaptic plasticity in vivo by imaging endogenous AMPA receptors and generates a detailed spatiotemporal map of synaptic changes during behavior.

This paper introduces TKIT, a CRISPR/Cas9 method for precise genomic knock-in in neurons, achieving up to 42% efficiency in mouse neurons and demonstrating its use in rat neurons for visualizing endogenous proteins.