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  • 1
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    Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. 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. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bosch, F -- Miksa, M -- Bittigau, P -- Vockler, J -- Dikranian, K -- Tenkova, T I -- Stefovska, V -- Turski, L -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):70-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/*cytology/drug effects/embryology/growth & development ; Calcium Channel Blockers/pharmacology ; Dizocilpine Maleate/pharmacology ; Dopamine Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Fetus ; Haloperidol/pharmacology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Electron ; Muscarinic Antagonists/pharmacology ; *Nerve Degeneration ; Neurons/*cytology/drug effects/metabolism ; Quinoxalines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/metabolism ; Scopolamine Hydrobromide/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: The deleterious effects of ethanol on the developing human brain are poorly understood. Here 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. Vulnerability coincides with the period of synaptogenesis, which in humans extends from the sixth month of gestation to several years after birth. During this period, transient ethanol exposure can delete millions of neurons from the developing brain. This can explain the reduced brain mass and neurobehavioral disturbances associated with human fetal alcohol syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bittigau, P -- Ishimaru, M J -- Wozniak, D F -- Koch, C -- Genz, K -- Price, M T -- Stefovska, V -- Horster, F -- Tenkova, T -- Dikranian, K -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1056-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite, Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Benzodiazepines/pharmacology ; Dose-Response Relationship, Drug ; Ethanol/administration & dosage/blood/*toxicity ; Female ; Fetal Alcohol Spectrum Disorders/*pathology ; GABA Modulators/pharmacology ; Humans ; *Nerve Degeneration ; Neurons/cytology/pathology ; Organ Size/drug effects ; Pregnancy ; Prosencephalon/cytology/*drug effects/embryology/growth & development ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A/*drug effects/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*drug effects/metabolism ; Synapses/drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Phencyclidine (PCP), a dissociative anesthetic and widely abused psychotomimetic drug, and MK-801, a potent PCP receptor ligand, have neuroprotective properties stemming from their ability to antagonize the excitotoxic actions of endogenous excitatory amino acids such as glutamate and aspartate. There is growing interest in the potential application of these compounds in the treatment of neurological disorders. However, there is an apparent neurotoxic effect of PCP and related agents (MK-801, tiletamine, and ketamine), which has heretofore been overlooked: these drugs induce acute pathomorphological changes in specific populations of brain neurons when administered subcutaneously to adult rats in relatively low doses. 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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Labruyere, J -- Price, M T -- DA 53568/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1360-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2660263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/cytology/*drug effects/pathology ; Dibenzocycloheptenes/*toxicity ; Dizocilpine Maleate ; Female ; Ketamine/toxicity ; Male ; Microscopy, Electron ; Neurons/drug effects ; Phencyclidine/*toxicity ; Rats ; Rats, Inbred Strains ; Tiletamine/toxicity ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    L-cysteine, a bicarbonate-sensitive endogenous excitotoxin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-04
    Description: After systemic administration to immature rodents, L-cysteine destroys neurons in the cerebral cortex, hippocampus, thalamus, and striatum, but the underlying mechanism has never been clarified. This neurotoxicity of L-cysteine, in vitro or in vivo, has now been shown to be mediated primarily through the N-methyl-D-aspartate subtype of glutamate receptor (with quisqualate receptor participation at higher concentrations). In addition, the excitotoxic potency of L-cysteine was substantially increased in the presence of physiological concentrations of bicarbonate ion. L-Cysteine is naturally present in the human brain and in the environment, and is much more powerful than beta-N-methylamino-L-alanine, a bicarbonate-dependent excitotoxin, which has been implicated in an adult neurodegenerative disorder endemic to Guam. Thus, the potential involvement of this common sulfur-containing amino acid in neurodegenerative processes affecting the central nervous system warrants consideration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Zorumski, C -- Price, M T -- Labruyere, J -- DA 05072/DA/NIDA NIH HHS/ -- HD 24237/HD/NICHD NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 May 4;248(4955):596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Washington University School of Medicine, Department of Psychiatry, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2185543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anticonvulsants/pharmacology ; Aspartic Acid/analogs & derivatives/pharmacology ; Bicarbonates/*pharmacology ; Caudate Nucleus/drug effects/*pathology ; Chick Embryo ; Cysteine/pharmacology/*toxicity ; Dibenzocycloheptenes/pharmacology ; Dizocilpine Maleate ; N-Methylaspartate ; Necrosis ; Neurons/drug effects/*pathology ; *Neurotoxins ; Rats ; Rats, Inbred Strains ; Retina/cytology/drug effects ; Retinal Ganglion Cells/cytology/drug effects ; Zinc/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    NMDA antagonist neurotoxicity: mechanism and prevention (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-06
    Description: Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, including phencyclidine (PCP) and ketamine, protect against brain damage in neurological disorders such as stroke. However, these agents have psychotomimetic properties in humans and morphologically damage neurons in the cerebral cortex of rats. It is now shown that the morphological damage can be prevented by certain anticholinergic drugs or by diazepam and barbiturates, which act at the gamma-aminobutyric acid (GABA) receptor-channel complex and are known to suppress the psychotomimetic symptoms caused by ketamine. Thus, it may be possible to prevent the unwanted side effects of NMDA antagonists, thereby enhancing their utility as neuroprotective drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Labruyere, J -- Wang, G -- Wozniak, D F -- Price, M T -- Sesma, M A -- AG 05681/AG/NIA NIH HHS/ -- DA 53568/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1835799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barbiturates/pharmacology ; Chick Embryo ; Dizocilpine Maleate/*antagonists & inhibitors ; Neurotoxins/*antagonists & inhibitors ; Parasympatholytics/pharmacology ; Pilocarpine/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*drug effects ; Scopolamine Hydrobromide/pharmacology ; Vacuoles/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-15
    Description: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate (a metabolite of the phosphoinositides, lipids involved in membrane receptor function) in the brain. The syndrome was preventable with atropine. The physostigmine doses and concentrations of blood lithium that caused the syndrome are similar to those considered appropriate for psychiatric chemotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Honchar, M P -- Olney, J W -- Sherman, W R -- MH-14677/MH/NIMH NIH HHS/ -- MH-38894/MH/NIMH NIH HHS/ -- NS-05159/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/pharmacology ; Brain Chemistry/drug effects ; Chlorides/adverse effects ; Drug Interactions ; Humans ; Inositol/analogs & derivatives/analysis ; *Inositol Phosphates ; Lithium/*adverse effects ; Lithium Chloride ; Male ; Parasympathomimetics/*adverse effects ; Physostigmine/adverse effects ; Pilocarpine/adverse effects ; Rats ; Rats, Inbred Strains ; Seizures/*chemically induced ; Substance-Related Disorders/*etiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Morphine analgesia potentiated but tolerance not affected by active immunization against cholecystokinin (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-12-07
    Description: Administration of cholecystokinin was recently found to attenuate opiate analgesia. In the present study, the role of endogenous cholecystokinin in opiate analgesia was examined. Endogenously released cholecystokinin was sequestered by antibodies to cholecystokinin developed in response to an active immunization procedure. Morphine analgesia was potentiated and prolonged in rats immunized against cholecystokinin. The rate of development of morphine tolerance, however, was not affected by the antibodies. Endogenous cholecystokinin appears to function as a short-term modulator of opiate action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faris, P L -- McLaughlin, C L -- Baile, C A -- Olney, J W -- Komisaruk, B R -- ES-07066/ES/NIEHS NIH HHS/ -- MH-38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1215-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Cholecystokinin/immunology/*physiology ; *Drug Tolerance ; Immunization ; Male ; Morphine/*pharmacology ; Pain/*physiology ; Rats ; Rats, Inbred Strains ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Focal cortical seizures cause distant thalamic lesions (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-10-08
    Description: Topical application of convulsants to the rat sensorimotor cortex in concentrations sufficient to cause repetitive focal motor seizures resulted in acute neuropathology (dark cell neuronal degeneration and spongiform neurophil changes) involving both the cortical seizure focus and certain thalamic nuclei within seizure pathways. Changes in the cortex were localized primarily in layer IV and those in the thalamus in nuclei having reciprocal connections with the cortical focus. The spongiform neuropil changes consisted of massively dilated presynaptic axon terminals in the cortex and postsynaptic dendrites in the thalamus. The dendritic and dark cell changes resemble the excitotoxic damage caused by glutamate and aspartate. Since these putative transmitters may be released locally from recurrent collaterals and remotely from corticothalamic axons, excessive release of glutamate or aspartate may account for the changes in both sites. The abnormal axons in sensory cortex appear to be terminals of thalamocortical neurons. Swelling of these axons may be caused by excessive anti- and orthodromic firing in the course of focal motor seizures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, R C -- Olney, J W -- MH-38894/MH/NIMH NIH HHS/ -- NS-09156/NS/NINDS NIH HHS/ -- NS-14834/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Oct 8;218(4568):177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7123229" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Cerebral Cortex/*physiopathology/ultrastructure ; Microscopy, Electron ; Neurons/physiology/ultrastructure ; Rats ; Rats, Inbred Strains ; Seizures/*physiopathology ; Thalamus/*physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Electronic Resource
    Electronic Resource
    Excitotoxic Amino Acids and Neuropsychiatric Disorders (1990)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 30 (1990), S. 47-71 
    Details
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.pa.30.040190.000403
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  • 10
    Electronic Resource
    Electronic Resource
    Nitrous oxide (laughing gas) is an NMDA antagonist, neuroprotectant and neurotoxin (1998)
    [s.l.] : Nature Publishing Group
    Nature medicine 4 (1998), S. 460-463 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Extensive research has failed to clarify the mechanism of action of nitrous oxide (N2O, laughing gas), a widely used inhalational anesthetic and drug of abuse. Other general anesthetics are thought to act by one of two mechanisms—blockade of NMDA glutamate receptors or enhancement of ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm0498-460
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