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Department of Pediatrics (E.T.), Wisconsin Regional Primate Research Center (E.T., D.L.F.), and Center for Neuroscience (E.T.), University of Wisconsin-Madison, Madison, Wisconsin 53715-1299
An increase in pulsatile release of LHRH is essential for the
onset of puberty. However, the mechanism controlling the pubertal
increase in LHRH release is still unclear. In primates the LHRH
neurosecretory system is already active during the neonatal period but
subsequently enters a dormant state in the juvenile/prepubertal period.
Neither gonadal steroid hormones nor the absence of facilitatory
neuronal inputs to LHRH neurons is responsible for the low levels of
LHRH release before the onset of puberty in primates. Recent studies
suggest that during the prepubertal period an inhibitory neuronal
system suppresses LHRH release and that during the subsequent
maturation of the hypothalamus this prepubertal inhibition is removed,
allowing the adult pattern of pulsatile LHRH release. In fact,
-aminobutyric acid (GABA) appears to be an inhibitory
neurotransmitter responsible for restricting LHRH release before the
onset of puberty in female rhesus monkeys. In addition, it appears that
the reduction in tonic GABA inhibition allows an increase in the
release of glutamate as well as other neurotransmitters, which
contributes to the increase in pubertal LHRH release. In this review,
developmental changes in several neurotransmitter systems controlling
pulsatile LHRH release are extensively reviewed.
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| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |