R. Ryley Parrish

This study shows that β-hydroxybutyrate can sustain brain tissue metabolism and function without glucose, demonstrating its role in maintaining neural activity during energy deprivation.

The paper introduces YSA, an open-source GUI for analyzing HD-MEA recordings, enabling efficient visualization and exploration of seizure dynamics in neural data.

The paper investigates whether blocking major inward cationic currents can prevent spreading depolarizations in zebrafish and mice, finding that these currents are not sufficient to block SD induction.

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 introduces an application to visualize mutations on voltage-gated sodium channels using D3.js, enabling customization and high-quality figure creation for genotype/phenotype studies.

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 investigates DNA 5-hydroxymethylation (5-hmC) changes in TLE patients and a rat model, finding reduced 5-hmC levels and specific gene associations, with Tet1 manipulation affecting seizure outcomes.

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

The paper determines the fractional block of Nav channels needed to impair neuronal excitability and reduce seizure-like activity using TTX in pyramidal neurons.

The paper introduces a GUI toolkit for analyzing LFP data from HD-MEA recordings, demonstrating its utility in detecting seizure propagation in Scn1aHet mice.

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

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.

This study shows that O-GlcNAc homeostasis is disrupted in TLE and that inhibiting OGA can reverse these changes and reduce seizures.