نتایج جستجو برای: excitotoxic neuronal damage

تعداد نتایج: 339314  

2016
Andrew J. Samson Graham Robertson Michele Zagnoni Christopher N. Connolly

Acute secondary neuronal cell death, as seen in neurodegenerative disease, cerebral ischemia (stroke) and traumatic brain injury (TBI), drives spreading neurotoxicity into surrounding, undamaged, brain areas. This spreading toxicity occurs via two mechanisms, synaptic toxicity through hyperactivity, and excitotoxicity following the accumulation of extracellular glutamate. To date, there are no ...

Journal: :Histology and histopathology 2003
M García E Vecino

Glial cells are thought to protect neurons from various neurological insults. When there is injury to retina, Müller cells, which are the predominant glial element in the retina, undergo significant morphological, cellular and molecular changes. Some of these changes reflect Müller cell involvement in protecting the retina from further damage. Müller cells express growth factors, neurotransmitt...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 1995
S B Churn D Limbrick S Sombati R J DeLorenzo

Neurotoxic effects of excitatory amino acids have been implicated in various neurological disorders, and have been utilized for excitotoxic models of delayed neuronal cell death. The excitotoxic glutamate-induced, delayed neuronal cell death also results in inhibition of calcium/calmodulin-dependent kinase II (CaM kinase II). In this report, we characterized the glutamate-induced inhibition of ...

2014
Parthiv Haldipur Nina Dupuis Vincent Degos Nicolas Moniaux Vibol Chhor Sowmyalakshmi Rasika Leslie Schwendimann Tifenn le Charpentier Elodie Rougier Paul Amouyal Gilles Amouyal Pascal Dournaud Christian Bréchot Vincent El Ghouzzi Jamila Faivre Bobbi Fleiss Shyamala Mani Pierre Gressens

OBJECTIVES Excitotoxicity plays a significant role in the pathogenesis of perinatal brain injuries. Among the consequences of excessive activation of the N-methyl-d-aspartate (NMDA)-type glutamate are oxidative stress caused by free radical release from damaged mitochondria, neuronal death and subsequent loss of connectivity. Drugs that could protect nervous tissue and support regeneration are ...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2005
Michael J O'Hare Neena Kushwaha Yi Zhang Hossein Aleyasin Steven M Callaghan Ruth S Slack Paul R Albert Inez Vincent David S Park

Cyclin-dependent kinase 5 (cdk5) is a member of the cyclin-dependent kinase family whose activity is localized mainly to postmitotic neurons attributable to the selective expression of its activating partners p35 and p39. Deregulation of cdk5, as a result of calpain cleavage of p35 to a smaller p25 form, has been suggested to be a central component of neuronal death underlying numerous neurodeg...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2010
Nikolaos Volakakis Banafsheh Kadkhodaei Eliza Joodmardi Karin Wallis Lia Panman Jessica Silvaggi Bruce M Spiegelman Thomas Perlmann

Induced expression of neuroprotective genes is essential for maintaining neuronal integrity after stressful insults to the brain. Here we show that NR4A nuclear orphan receptors are induced after excitotoxic and oxidative stress in neurons, up-regulate neuroprotective genes, and increase neuronal survival. Moreover, we show that NR4A proteins are induced by cAMP response element binding protein...

1999
Joshua L. Roffman Barbara K. Lipska Alessandro Bertolino Peter Van Gelderen Alan W. Olson Daniel R. Weinberger

Introduction The prefrontal cortex (PFC) and the dopaminergic system have been implicated in the pathophysiology of schizophrenia. However, how these two neuronal systems interact with each other is not fully understood. Previous studies in rats have indicated that the PFC regulates the firing of dopamine (DA) neurons as well as DA-related behaviors through projections to subcortical areas incl...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 1998
H Xiang Y Kinoshita C M Knudson S J Korsmeyer P A Schwartzkroin R S Morrison

The tumor suppressor gene p53 has been implicated in the loss of neuronal viability, but the signaling events associated with p53-mediated cell death in cortical and hippocampal neurons are not understood. Previous work has shown that adenovirus-mediated delivery of the p53 gene causes cortical and hippocampal neuronal cell death with some features typical of apoptosis. In the present study we ...

2010
Jessie Irene Luoma

......................................................................................................................... i List of Tables................................................................................................................ v List of Figures.............................................................................................................. iv Chapter One: In...

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