Andrew J. Trevelyan

This study shows that spreading depolarizations (SDs) are associated with seizure termination in both human and rodent models, with SDs reducing seizure duration and delaying subsequent events.

The paper uses RNA sequencing to analyze transcriptomic changes in mouse neocortical tissue exposed to epileptiform activity, identifying gene expression alterations linked to epilepsy.

The paper shows that two optogenetic ion pumps, halorhodopsin and archaerhodopsin, cause different secondary K+ redistribution patterns after activation.

The paper demonstrates an in vitro human brain model to study STXBP1 haploinsufficiency's effects on synaptic connectivity and cortical development.

This study identifies a novel anticonvulsant compound that targets neuronal homeostasis by increasing Pumilio expression, showing efficacy in Drosophila and mouse seizure models.

This study shows that reducing PGC-1α in PV interneurons decreases seizure-like activity in an acute epilepsy model by limiting interneuron firing intensity.

The paper shows that intracellular chloride levels in cortical pyramidal cells vary diurnally, affecting neuronal network stability and seizure latency.

The paper measures light penetration through rodent brain tissue using nucleated patches and direct visualization, finding a lower extinction coefficient than previous estimates.

The paper identifies synergistic positive feedback mechanisms that drive seizure initiation and shows that an optogenetic stimulation paradigm can delay epileptic activity.

The paper develops a novel spike sorting method to analyze neuronal activity during human seizures, finding that recruited neurons show altered action potential waveforms compared to non-recruited tissue.

The paper develops computational models to show how chloride dynamics affect neuronal input-output functions through changes in dendritic inhibition.

The paper analyzes seizure network dynamics in focal epilepsy patients, finding that seizure pathways change on circadian and slower timescales, independent of medication.

The paper shows that parvalbumin-expressing interneurons propagate activity through gap-junctions when extracellular K+ rises, which is relevant to seizure dynamics.

The paper compares two in vitro models of epileptic seizures, finding differences in glutamatergic involvement and seizure-like event characteristics.

The paper investigates the cellular mechanisms of benzodiazepine resistance in status epilepticus, finding that persistent high intraneuronal chloride levels contribute to reduced GABAA receptor function and enhanced epileptiform activity.

The paper shows that epileptiform activity transitions in vitro arise from shifts in ictal sources, with hippocampal activity entraining other cortical areas through non-synaptic mechanisms.