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Kim L. Powell

Researcher at Monash University

Publications -  54
Citations -  2068

Kim L. Powell is an academic researcher from Monash University. The author has contributed to research in topics: Epilepsy & Epileptogenesis. The author has an hindex of 19, co-authored 52 publications receiving 1730 citations. Previous affiliations of Kim L. Powell include University of Melbourne & Australian National University.

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The P2X7 Receptor Drives Microglial Activation and Proliferation: A Trophic Role for P2X7R Pore

TL;DR: It is reported that overexpression alone of a purinergic P2x7R, in the absence of pathological insults, is sufficient to drive the activation and proliferation of microglia in rat primary hippocampal cultures and evidence is provided for a novel trophic role for P2X7R pore inmicroglia.
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T-Type Calcium Channel Blockers That Attenuate Thalamic Burst Firing and Suppress Absence Seizures

TL;DR: The ability of the T-type Ca2+ channel antagonists to inhibit absence seizures and to reduce the duration and cycle frequency of spike-and-wave discharges suggests that these agents have a unique mechanism of action on pathological thalamocortical oscillatory activity distinct from current drugs used in clinical practice.
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A Cav3.2 T-Type Calcium Channel Point Mutation Has Splice-Variant-Specific Effects on Function and Segregates with Seizure Expression in a Polygenic Rat Model of Absence Epilepsy

TL;DR: A homozygous, missense, single nucleotide (G to C) mutation in the Cav3.2 T-type Ca2+ channel gene (Cacna1h) in the genetic absence epilepsy rats from Strasbourg (GAERS) model has a novel mechanism of action, being dependent on exonic splicing for its functional consequences to be expressed.
Journal Article

A cav3.2 t-type calcium channel point mutation has splice variant-specific effects on function and segregates with seizure expression in a polygenic rat model of absence epilepsy

TL;DR: In this paper, a homozygous, missense, single nucleotide (G to C) mutation in the Cav3.2 T-type Ca2+ channel gene (Cacna1h) in the genetic absence epilepsy rats from Strasbourg (GAERS) model was described.
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Glutamate is associated with a higher risk of seizures in patients with gliomas

TL;DR: In this article, the authors investigated the relationship of glutamate and glutamate transporter expression in human gliomas and surrounding peritumoral brain to the presence of tumor-associated seizures.