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Selective Antagonism of GluR5 Kainate-Receptor-Mediated Synaptic Currents by Topiramate in Rat Basolateral Amygdala Neurons
In whole-cell voltage-clamp recordings from principal neurons of the rat basolateral amygdala, topiramate selectively inhibited pharmacologically isolated excitatory synaptic currents mediated by kainate receptors containing the GluR5 subunit, supporting the concept that GLUR5 kainates receptors represent a novel target for antiepileptic drug development.
Adult Murine Skeletal Muscle Contains Cells That Can Differentiate into Beating Cardiomyocytes In Vitro
A novel population of nonsatellite cells in adult murine skeletal muscle that progress under standard primary cell-culture conditions to autonomously beating cardiomyocytes, characterized here by video microscopy, confocal-detected calcium transients, electron microscope, and immunofluorescent cardiac-specific markers.
GluR5 Kainate Receptors, Seizures, and the Amygdala
- M. Rogawski, Divina S. Gryder, D. Castañeda, W. Yonekawa, M. K. Banks, He Li
- Biology, PsychologyAnnals of the New York Academy of Sciences
- 1 April 2003
Observations indicate that GluR5 kainate receptors have a unique role in triggering epileptiform activity in the amygdala and could participate in long‐term plasticity mechanisms that underlie some forms of epileptogenesis.
NNZ-2566, a Glypromate Analog, Attenuates Brain Ischemia-Induced Non-Convulsive Seizures in Rats
- X. Lu, Y. Si, A. Williams, J. Hartings, Divina S. Gryder, F. Tortella
- Biology, MedicineJournal of cerebral blood flow and metabolism…
- 29 July 2009
Results indicate that NNZ-2566 possesses a unique therapeutic potential as a safe prophylactic agent that synergistically provides neuroprotection and reduces injury-induced seizures.
Topiramate reduces non-convulsive seizures after focal brain ischemia in the rat
Evidence for low GluR2 AMPA receptor subunit expression at synapses in the rat basolateral amygdala
Although BLA principal neurons express perikaryal and proximal dendritic GluR2 immunoreactivity, few synapses onto these neurons express Glu R2, and a preponderance of principal neurons have inwardly rectifying AMPA‐mediated synaptic currents, suggesting that targeting of Glur2 to synapses is restricted.