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Role of Peroxidase-Positive Astrocytes in Estradiol-Related Hypothalamic Damage

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Biology and Pathology of Astrocyte-Neuron Interactions

Part of the book series: Altschul Symposia Series ((ALSS,volume 2))

Abstract

Astrocytes perform a wide range of adaptive functions in the mammalian nervous system including maintenance of the blood-brain barrier and ion homeostasis, sequestration and metabolism of various neurotransmitters, antigen presentation to immunocytes and elaboration of a scaffolding for neuronal migration during embryogenesis (Fedoroff & Vernadakis, 1986A; Wilkin et al., 1990). On the other hand, astrocytes may, under certain circumstances, mediate dystrophic effects within the CNS and thereby contribute to a decline in neurologic function. Examples of the latter include formation of epileptogenic scar tissue following CNS injury, neoplastic transformation and malignant behaviour, metabolism of protoxins (such as MPTP) to potent neurotoxins (MPP+), and accumulation and release of excitotoxic amino acids during tissue hypoxia and aluminum exposure (Fedoroff & Vernadakis 1986B; Langston 1985; Tholey et al 1991; Albrecht et al., 1991). In this article, I review evidence implicating a subpopulation of astrocytes replete with redox-active iron in the pathogenesis of estrogen-related hypothalamic damage and anovulatory sterility in rodents.

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Authors and Affiliations

  1. Department of Neurology, McGill University, USA

    Hyman M. Schipper

  2. Lady Davis Institute for Medical Research, Sir Mortimer B. Davis — Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec, H3T 1E2, Canada

    Hyman M. Schipper

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  1. University of Saskatchewan, Saskatoon, Saskatchewan, Canada

    Sergey Fedoroff , Bernhard H. J. Juurlink  & Ronald Doucette ,  & 

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Schipper, H.M. (1993). Role of Peroxidase-Positive Astrocytes in Estradiol-Related Hypothalamic Damage. In: Fedoroff, S., Juurlink, B.H.J., Doucette, R. (eds) Biology and Pathology of Astrocyte-Neuron Interactions. Altschul Symposia Series, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9486-1_11

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  • DOI: https://doi.org/10.1007/978-1-4757-9486-1_11

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