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Some Hypothalamic Hamartomas Contain Transforming Growth Factor , a Puberty-Inducing Growth Factor, But Not Luteinizing Hormone-Releasing Hormone Neurons¹

Division of Neuroscience (H.J., M.E.C., A.C., Y.J.M., S.R.O.), Oregon Regional Primate Research Center/Oregon Health Sciences University, Beaverton, Oregon, 97006; Clinics of Pediatrics (H.J., K.H.P.B.) and Neurosurgery (M.W.), University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany; Center for Neurological Surgery (P.C.) and Division of Pediatric Endocrinology (M.S.S.), UMDNJ, New Jersey Medical School, Newark, New Jersey 07103-2499; Department of Anatomy and Cell Biology (J.W.W.), College of Physicians and Surgeons, Columbia University, New York, New York 10032; and Departments of Neurosurgery and Pediatrics (J.H.P.), Oregon Health Sciences University, Portland, Oregon 97201-3098

Address correspondence and requests for reprints to: Sergio R. Ojeda, Division of Neuroscience/Oregon Regional Primate Research Center, Oregon Health Sciences University, 505 NW 185th Avenue, Beaverton, Oregon 97006.

Activation of LH-releasing hormone (LHRH) secretion, essential for the initiation of puberty, is brought about by the interaction of neurotransmitters and astroglia-derived substances. One of these substances, transforming growth factor (TGF), has been implicated as a facilitatory component of the glia-to-neuron signaling process controlling the onset of female puberty in rodents and nonhuman primates. Hypothalamic hamartomas (HH) are tumors frequently associated with precocious puberty in humans. The detection of LHRH-containing neurons in some hamartomas has led to the concept that hamartomas advance puberty because they contain an ectopic LHRH pulse generator. Examination of two HH associated with female sexual precocity revealed that neither tumor had LHRH neurons, but both contained astroglial cells expressing TGF and its receptor. Thus, some HH may induce precocious puberty, not by secreting LHRH, but via the production of trophic factors—such as TGF—able to activate the normal LHRH neuronal network in the patient’s hypothalamus.

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