Abstract:
:The long-acting opiate antagonist naltrexone hydrochloride was administered by intraperitoneal injection, in a dose response protocol, to adult rats. The drug was used to observe effects of opiate receptor blockade on cells of the pituitary gland and adjacent hypothalamus. At higher drug doses (5 mg/kg or 10 mg/kg), neurites directly innervating pars intermedia cells contained swollen vesicles and disrupted membranous elements. Fibers within the median eminence of the hypothalamus appeared swollen, and contained myelin figures. Despite the consistent degenerative changes appearing in neurites, measurements of levels of dopamine, norepinephrine, and epinephrine in striatum, and hypothalamus did not differ significantly between naltrexone-treated or control animals, although there was a significant elevation of norepinephrine in the pituitary after drug treatment. At all drug dose levels administered, supraependymal neuron-like cells appeared atop the ependyma of the third ventricle above the median eminence. These observations suggest that naltrexone produces specific "neurotoxic" effects on neurites of the tuberoinfundibular system, and may induce changes in the ventricular environment which stimulate the appearance of supraependymal neurons.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Saland LC,Reyes E,Ortiz Edoi
10.1007/BF00964168subject
Has Abstractpub_date
1984-02-01 00:00:00pages
207-17issue
2eissn
0364-3190issn
1573-6903journal_volume
9pub_type
杂志文章abstract::This study was undertaken to evaluate whether chemical hypoxia-induced cell injury is a result of reactive oxygen species (ROS) generation, ATP depletion, mitochondrial permeability transition, and an increase in intracellular Ca2+, in A172 cells, a human glioma cell line. Chemical hypoxia was induced by incubating ce...
journal_title:Neurochemical research
pub_type: 杂志文章
doi:10.1023/a:1024280429036
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journal_title:Neurochemical research
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doi:10.1007/BF00964144
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pub_type: 杂志文章,评审
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journal_title:Neurochemical research
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journal_title:Neurochemical research
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doi:10.1007/s11064-015-1782-z
更新日期:2016-05-01 00:00:00
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journal_title:Neurochemical research
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更新日期:2005-09-01 00:00:00
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更新日期:2008-01-01 00:00:00
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更新日期:2008-07-01 00:00:00
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journal_title:Neurochemical research
pub_type: 杂志文章
doi:10.1007/BF00964358
更新日期:1978-02-01 00:00:00
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abstract::Traumatic brain injury (TBI) initiates a series of neurochemical and signaling changes that could eventually lead to neuronal apoptosis. Recent studies indicated that mature neurons cell cycle re-enter played a crucial role in neuronal apoptosis. In this study, we identified that the chaperonin containing TCP-1, subun...
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journal_title:Neurochemical research
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更新日期:2004-04-01 00:00:00
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更新日期:1990-06-01 00:00:00
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journal_title:Neurochemical research
pub_type: 杂志文章
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更新日期:2020-08-01 00:00:00
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