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Endocrinology Vol. 142, No. 5 2078-2086
Copyright © 2001 by The Endocrine Society

ARTICLES

Nerve Growth Factor Is Required for Early Follicular Development in the Mammalian Ovary1

Gregory A. Dissen, Carmen Romero2, Anne Newman Hirshfield and Sergio R. Ojeda

Division of Neuroscience (G.A.D., C.R., S.R.O.), Oregon Regional Primate Research Center/Oregon Health Science University, Beaverton, Oregon 97006-3448; and Department of Anatomy and Cell Biology (A.N.H.), University of Maryland, Baltimore, Maryland 21202

Address all correspondence and requests for reprints to: Sergio R. Ojeda, Division of Neuroscience, Oregon Regional Primate Research Center, 505 NW 185th Avenue, Beaverton, Oregon 97006-3448. E-mail: ojedas{at}ohsu.edu

Nerve growth factor (NGF) epitomizes a family of proteins known as the neurotrophins (NTs), which are required for the survival and differentiation of neurons within both the central and peripheral nervous system. Synthesis of NGF in tissues innervated by the peripheral nervous system is consistent with its function as a target-derived trophic factor. However, the presence of low- and high-affinity NGF receptors in the gonads suggests another function for the NTs within the reproductive endocrine system. We now report that NGF is required for the growth of primordial ovarian follicles, a process known to occur independently of pituitary gonadotropins. Both the NT receptor p75NTR and the NGF tyrosine kinase receptor trkA were found to be expressed in the ovaries of infantile normal mice and mice carrying a null mutation of the NGF gene. The ovaries from homozygote NGF-null (-/-) mutant animals, analyzed after completion of ovarian histogenesis, exhibited a markedly reduced population of primary and secondary follicles in the presence of normal serum gonadotropin levels, and an increased number of oocytes that failed to be incorporated into a follicular structure. Assessment of mitogenic activity using two complementary proliferation markers revealed a conspicuous reduction in somatic cell proliferation in the ovaries of NGF-deficient mice. These results suggest that the delay in follicular growth observed in NGF-/- mice may be related to the loss of a proliferative signal provided by NGF to the nonneural endocrine component of the ovary.




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