Sam A. Booker

The paper shows that GABAB receptor activation in SST interneurons leads to PP2A-dependent internalization, affecting plasticity and disrupting contextual memory.

This study shows that FMRP depletion in human neurons causes cyclic-AMP-dependent hyperexcitability, which can be corrected by inhibiting phosphodiesterase 4D.

The paper tests for axon initial segment (AIS) structural plasticity in human, mouse, and rat cortical neurons across different conditions and finds no evidence of AIS length changes over short-term activity modulation.

This study uses live human brain slice cultures to show that physiological and pathological amyloid-beta have opposing effects on synapses, with physiological levels enhancing synaptic transcripts and pathological levels causing synaptic loss.

This study shows that noradrenergic modulation can restore visual discrimination in a SYNGAP1 mouse model by improving coding precision in the primary visual cortex.

This study shows that neurodevelopmental processes in the cortex and thalamus can occur normally without microglia, using a genetically modified mouse model.

The paper shows that hyperpolarization-activated currents (Ih) generate sequential neuronal activation patterns in the mouse head-direction cortex during sleep.

This study quantifies how GABAB receptor signalling contributes to circuit-level inhibition in rat and human cortical principal cells across the lifespan, revealing age and species differences.

This study shows that rats with Fragile X Syndrome exhibit impaired experience-dependent changes in hippocampal spatial activity and circuit function compared to wild-type rats.

The paper identifies developing interneurons as a potential target for autism genetic risk factors by analyzing human and rodent neural data.

LAB-AID is an interactive web tool that visualizes and interrogates hierarchical biological experimental data to improve understanding and identify outliers and batch effects.

This paper investigates whether demyelination in multiple sclerosis leads to selective neurodegeneration of inhibitory interneurons and presents a rodent model to study this phenomenon.

This study shows that loss of FMRP in a mouse model of Fragile X Syndrome leads to increased single-spine excitation and more multiply-innervated spines, contributing to circuit hyperexcitability.

The paper investigates how cellular and synaptic compensations in Fmr1-KO mice affect sensory processing in the barrel cortex, finding that despite compensatory mechanisms, sensory encoding precision is lost, leading to hypersensitivity.