Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.
- C. Ikonomidou, P. Bittigau, J. Olney
- Biology, MedicineScience
- 11 February 2000
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.
Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.
- C. Ikonomidou, F. Bosch, J. Olney
- Biology, MedicineScience
- 1999
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.
Glutamate receptor dysfunction and schizophrenia.
It is proposed that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents, a better understanding of this mechanism may lead to improved pharmacotherapy in schizophrenia.
Early Exposure to Common Anesthetic Agents Causes Widespread Neurodegeneration in the Developing Rat Brain and Persistent Learning Deficits
- V. Jevtovic-Todorovic, R. Hartman, D. Wozniak
- BiologyJournal of Neuroscience
- 1 February 2003
A combination of drugs commonly used in pediatric anesthesia in doses sufficient to maintain a surgical plane of anesthesia is administered to 7-d-old infant rats, and it is observed that this causes widespread apoptotic neurodegeneration in the developing brain, deficits in hippocampal synaptic function, and persistent memory/learning impairments.
NMDA receptor hypofunction model of schizophrenia.
- J. Olney, J. Newcomer, N. Farber
- Psychology, MedicineJournal of Psychiatric Research
- 1 November 1999
Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate
- J. Olney
- Medicine, BiologyScience
- 9 May 1969
It is postulated that the aduls syndrome represents a multifacted nueroendocrine disturbance arising from the disruption of developing nueral centers concered in the mediation of endocrine function.
Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.
- J. Olney, J. Labruyere, M. Price
- Biology, PsychologyScience
- 16 June 1989
These findings raise new questions regarding the safety of these agents in the clinical management of neurodegenerative diseases and reinforce concerns about the potential risks associated with illicit use of PCP.
Glutamate and the pathophysiology of hypoxic–ischemic brain damage
- S. Rothman, J. Olney
- BiologyAnnals of Neurology
- 1 February 1986
It is suggested that glutamate plays a key role in ischemic brain damage, and that drugs which decrease the accumulation of glutamate or block its postsynaptic effects may be a rational therapy for stroke.
Antiepileptic drugs and apoptotic neurodegeneration in the developing brain
- P. Bittigau, M. Sifringer, C. Ikonomidou
- Biology, PsychologyProceedings of the National Academy of Sciences…
- 4 November 2002
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.
Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease.
- D. Holtzman, K. Bales, S. Paul
- BiologyProceedings of the National Academy of Sciences…
- 14 March 2000
The data demonstrate a critical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD.
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