quisqualic acid/atrophy

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Neuronal degeneration and spinal cavitation following intraspinal injections of quisqualic acid in the rat.

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Microinjections of quisqualic acid were made in the spinal cord to evaluate the excitotoxic effects of this excitatory amino acid agonist on spinal neurons in the rat. Animals were divided into four groups based on post injection survival times of 7-49 days. Injections ranging from 0.3 to 2.0 microL

Idebenone attenuates neuronal degeneration induced by intrastriatal injection of excitotoxins.

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Previous studies with the N18-RE-105 neuronal-like cell line and primary cortical cultures demonstrate that glutamate can produce a calcium-dependent, delayed form of neuronal degeneration that results from its competitive inhibition of cystine transport, which leads to cellular glutathione

[Epileptogenic properties of quisqualic acid: microinjection into the unilateral amygdala in cats].

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The present studies demonstrated that the microinjection of quisqualic acid (QA) into unilateral amygdala in chronically implanted cats resulted in various types of limbic seizures in accordance with injected doses. The epileptogenic potency of QA in the induction of epileptic seizures was lower

Quisqualic acid-induced lesion of the nucleus basalis of Meynert in young and aging rats: plasticity of surviving NGF receptor-positive cholinergic neurons.

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Previous studies have demonstrated that cholinergic neurons in the adult rat forebrain, i.e., septal region, are able to respond and regenerate after damage followed by exogenous treatment with beta-nerve growth factor. Furthermore, it has been shown that an age-related loss of NGF-receptor (NGFr)

C-fos expression in the rat nucleus basalis upon excitotoxic lesion with quisqualic acid: a study in adult and aged animals.

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A unilateral quisqualic acid lesion was placed in the nucleus basalis magnocellularis of 3- and 24-month-old rats, and the animals were sacrificed at different times post-surgery. The morphology and the number of the cholinergic neurons of the nucleus basalis were analyzed by means of

CGS-19755 and MK-801 selectively prevent rat striatal cholinergic and gabaergic neuronal degeneration induced by N-methyl-D-aspartate and ibotenate in vivo.

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The in vivo efficacies and potencies of various excitatory amino acid agonists in inducing cholinergic neuronal degeneration were compared following unilateral injections into the rat striatum. Kainic acid (KA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), ibotenic acid (IBO),

The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo.

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Brain inflammatory processes underlie the pathogenesis of Alzheimer's disease, and non-steroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this work was to study in vivo whether attenuation of brain inflammatory response to excitotoxic insult by the selective

Brain inflammatory reaction in an animal model of neuronal degeneration and its modulation by an anti-inflammatory drug: implication in Alzheimer's disease.

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Brain inflammatory processes underlie the pathogenesis of Alzheimer's disease, and nonsteroidal anti-inflammatory drugs have a protective effect in the disease. The aim of this study was to characterize in vivo in the rat brain the inflammatory reaction in response to excitotoxic insult and to

Kainic acid: insights into excitatory mechanisms causing selective neuronal degeneration.

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Kainic acid, an acidic pyrolidine isolated from the seaweed Digenea simplex, is the most potent of the commonly used exogenous excitotoxins. The neurotoxic threshold of kainic acid is nearly two magnitudes lower than that of the other receptor-specific agonists, N-methyl-D-aspartic acid and

Differential brain area vulnerability to long-term subcortical excitotoxic lesions.

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To investigate the long-term effects of excitatory amino acid microinjections into the basal forebrain and its correlation with a possible Ca2+ imbalance associated with the excitotoxic process, ibotenic acid, mainly an N-methyl-D-aspartate receptor agonist, and quisqualic acid, an agonist of

The effects of excitatory amino acids on intracellular calcium in single mouse striatal neurons in vitro.

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Using microspectrofluorimetry and the calcium-sensitive dye fura-2, we examined the effect of excitatory amino acids on [Ca2+]i in single striatal neurons in vitro. N-methyl-D-aspartic acid (NMDA) produced rapid increases in [Ca2+]i. These were blocked by DL-2-amino-5-phosphonovaleric acid (AP5), by

[Epileptogenicity and neurotoxicity induced by intra-amygdaloid injection of various excitatory amino acids in rats].

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The electroencephalographic and histopathological changes following intra-amygdaloid injection of excitatory amino acids were examined in rats. Limbic seizure status was induced after injection of kainic acid (KA), domoic acid (DA), quisqualic acid (QA), alpha-allo-kainic acid (ALLO-KA) and

Short-term and complete reversal of NGF effects in rats with lesions of the nucleus basalis magnocellularis.

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Rats received bilateral quisqualic acid lesions of the nucleus basalis magnocellularis. Three weeks after lesioning, osmotic minipumps were implanted that released recombinant human nerve growth factor or cytochrome c at a dosage of 5.0 microg rat-1 day-1 through intracerebroventricular cannulas for

Molecular cloning, functional expression, pharmacological characterization and chromosomal localization of the human metabotropic glutamate receptor type 3.

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Glutamic acid is the major excitatory amino acid of the central nervous system which interacts with two receptor families, the ionotropic and metabotropic glutamate receptors. The metabotropic glutamate receptors (mGluRs) are coupled to G proteins and can be divided into three subgroups based on

Morphology of quisqualate-induced neurotoxicity in the chicken retina.

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In this study, the acute neurotoxic effects of quisqualic acid on the chick retina were examined 2 hr or 2 days following intravitreal injections of either 100 or 200 nmol quisqualic acid (QUIS). Both doses resulted in marked nuclear pyknosis and cytoplasmic swelling of a large population of cells

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