17β-estradiol protects male mice from cuprizone-induced demyelination and oligodendrocyte loss

Lorelei C. Taylor; Kasturi Puranam; Wendy Gilmore; Jenny P-Y. Ting; Glenn K. Matsushima

Neurobiology of Disease (Aug 2010)

17β-estradiol protects male mice from cuprizone-induced demyelination and oligodendrocyte loss

Lorelei C. Taylor,
Kasturi Puranam,
Wendy Gilmore,
Jenny P-Y. Ting,
Glenn K. Matsushima

Affiliations

Lorelei C. Taylor: Curriculum in Neurobiology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina-CH, Chapel Hill, NC 27599, USA
Kasturi Puranam: UNC Neuroscience Center, University of North Carolina-CH, Chapel Hill, NC 27599, USA
Wendy Gilmore: Department of Neurology, University of Southern California, Los Angeles, CA 90033, USA
Jenny P-Y. Ting: Curriculum in Neurobiology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; UNC Neuroscience Center, University of North Carolina-CH, Chapel Hill, NC 27599, USA
Glenn K. Matsushima: Curriculum in Neurobiology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; UNC Neuroscience Center, University of North Carolina-CH, Chapel Hill, NC 27599, USA; Program for Molecular Biology and Biotechnology, University of North Carolina-CH, Chapel Hill, NC 27599, USA; Corresponding author. University of North Carolina, 115 Mason Farm Rd, CB# 7250, Chapel Hill, NC 27599, USA. Fax: +1 919 966 9605.

Journal volume & issue: Vol. 39, no. 2
pp. 127 – 137

Abstract

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In addition to regulating reproductive functions in the brain and periphery, estrogen has tropic and neuroprotective functions in the central nervous system (CNS). Estrogen administration has been demonstrated to provide protection in several animal models of CNS disorders, including stroke, brain injury, epilepsy, Parkinson's disease, Alzheimer's disease, age-related cognitive decline and multiple sclerosis. Here, we use a model of toxin-induced oligodendrocyte death which results in demyelination, reactive gliosis, recruitment of oligodendrocyte precursor cells and subsequent remyelination to study the potential benefit of 17β-estradiol (E2) administration in male mice. The results indicate that E2 partially ameliorates loss of oligodendrocytes and demyelination in the corpus callosum. This protection is accompanied by a delay in microglia accumulation as well as reduced mRNA expression of the pro-inflammatory cytokine, tumor necrosis factor alpha (TNFα), and insulin-like growth factor-1 (IGF-1). E2 did not significantly alter the accumulation of astrocytes or oligodendrocyte precursor cells, or remyelination. These data obtained from a toxin-induced, T cell-independent model using male mice provide an expanded view of the beneficial effects of estrogen on oligodendrocyte and myelin preservation.

Published in Neurobiology of Disease

ISSN: 0969-9961 (Print); 1095-953X (Online)
Publisher: Elsevier
Country of publisher: United States
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.journals.elsevier.com/neurobiology-of-disease

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