Abstract
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 α (TGFα), 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 TGFα and its receptor. Thus, some HH may induce
precocious puberty, not by secreting LHRH, but via the production of
trophic factors—such as TGFα—able to activate the normal LHRH
neuronal network in the patient’s hypothalamus.