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Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.
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. Expand
Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.
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. Expand
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. Expand
Early Exposure to Common Anesthetic Agents Causes Widespread Neurodegeneration in the Developing Rat Brain and Persistent Learning Deficits
- V. Jevtovic-Todorovic, R. Hartman, +5 authors D. Wozniak
- The Journal 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. Expand
NMDA receptor hypofunction model of schizophrenia.
A version of the NMDA receptor hypofunction hypothesis that has evolved from recent studies pertaining to the neurotoxic and psychotomimetic effects of PCP and related NMDA antagonist drugs is presented. Expand
Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.
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. Expand
Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate
- J. Olney
- 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. Expand
Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis
- J. Newcomer, N. Farber, +5 authors J. Olney
- Psychology, Medicine
- 1 February 1999
This double-blind, placebo-controlled, randomized, within-subjects comparison of three fixed subanesthetic, steady-state doses of intravenous ketamine in healthy males demonstrated dose-dependent increases in Brief Psychiatric Rating Scale positive and negative symptoms. Expand
Glutamate and the pathophysiology of hypoxic–ischemic brain damage
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. Expand