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Animal Models of Brain Hypoxia

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Part of the book series: Neuromethods ((NM,volume 22))

Abstract

Hypoxia (i.e., reduced oxygen availability) is a classical model of the metabolic encephalopathies or delirium. An understanding of how hypoxia alters brain function has implications for understanding other metabolic encephalopathies as well as aging and age-related disorders, such as Alzheimer’s disease. Utilizing a variety of models of hypoxia is necessary to determine the effects of hypoxia on brain function and to test hypotheses about the underlying mechanisms of its actions. Both in vivo and in vitro models of hypoxia are produced by either limiting the oxygen availability or impairing the tissues′ ability to utilize oxygen. The results demonstrate that the synthesis and release of neurotransmitters are particularly sensitive to hypoxia. The release of acetylcholine is diminished, whereas the release of dopamine and glutamate is accelerated. We postulate that diminished acetylcholine release impairs mental function, whereas the excessive release of dopamine and glutamate damages cells postsynaptically. Fundamental alterations in calcium homeostasis, particularly the ability of mitochondria to buffer calcium, appear to underlie these deficits. Furthermore, these changes in calcium appear to affect other second messenger systems, including an acceleration of the phosphatidylinositol cascade

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Gibson, G.E., Huang, HM. (1992). Animal Models of Brain Hypoxia. In: Boulton, A.A., Baker, G.B., Butterworth, R.F. (eds) Animal Models of Neurological Disease, II. Neuromethods, vol 22. Humana Press. https://doi.org/10.1385/0-89603-211-6:51

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  • DOI: https://doi.org/10.1385/0-89603-211-6:51

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