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Chrysanthy Ikonomidou

Researcher at University of Wisconsin-Madison

Publications -  111
Citations -  13088

Chrysanthy Ikonomidou is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Neurodegeneration & Glutamate receptor. The author has an hindex of 54, co-authored 105 publications receiving 12311 citations. Previous affiliations of Chrysanthy Ikonomidou include Washington University in St. Louis & Dresden University of Technology.

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Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.

TL;DR: Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival.
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Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.

TL;DR: It is reported that ethanol, acting by a dual mechanism [blockade of N-methyl-D-aspartate (NMDA) glutamate receptors and excessive activation of GABA(A) receptors], triggers widespread apoptotic neurodegeneration in the developing rat forebrain.
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Antiepileptic drugs and apoptotic neurodegeneration in the developing brain.

TL;DR: It is revealed that phenytoin, phenobarbital, diazepam, clonazepam, vigabatrin, and valproate cause apoptotic neurodegeneration in the developing rat brain at plasma concentrations relevant for seizure control in humans.
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Long-term effects of pilocarpine in rats: structural damage of the brain triggers kindling and spontaneous recurrent seizures.

TL;DR: It is demonstrated that structural damage of the brain may lead to spontaneously recurrent convulsions (chronic epilepsy) in rats and that kindling mechanisms underlie the development of epileptic foci from structural brain lesions, which suggests thatkindling mechanisms may be involved in the etiology of some forms of epilepsy in humans.
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Review: Cholinergic mechanisms and epileptogenesis. The seizures induced by pilocarpine: A novel experimental model of intractable epilepsy

TL;DR: The amygdala, thalamus, olfactory cortex, hippocampus, neocortex, and substantia nigra are the most sensitive regions to epilepsy‐related damage following convulsions produced by pilocarpine.