The rat preoptic area-anterior hypothalamic continuum (POA-AH) contains about 400-800 neurons that express the decapeptide
GnRH and the 56-amino-acid
GnRH-associated peptide. Originating from the olfactory placode, these neurons migrate and establish their final distribution and connections in the POA-AH several days before birth. The aim of the present study was to examine whether the biosynthesis of the
mRNA encoding the precursor (
proGnRH) common to
GnRH and
GnRH-associated peptide undergoes postnatal changes corresponding to the development of sexual maturation. The POA-AH content of
proGnRH messenger RNA (
mRNA) was followed from postnatal day 1 to day 90 in female and male Sprague-Dawley rats killed by
decapitation between 1000-1200 h. Cytoplasmic
RNA fractionated from individual POA-AH homogenates was purified using
proteinase K digestion. Cytoplasmic
proGnRH mRNA was quantitated simultaneously with
cyclophilin mRNA (an internal standard control) using
solution hybridization-
RNase protection assay, with the protected fragments separated through
polyacrylamide gel electrophoresis. In the POA-AH, the concentrations of
proGnRH mRNA (femtograms
mRNA per microgram total
RNA) increased significantly with age in both sexes (P less than 0.001). In males,
proGnRH mRNA levels increased by day 30 some 2-fold over the values of days 5 and 10, and the levels established on day 30 were maintained through adulthood. In females, the first rise in
proGnRH mRNA levels occurred on day 30, followed by an additional increase on day 45 to levels seen in adulthood. Levels of
proGnRH mRNA established in adulthood were significantly higher in females than in males (P less than 0.03). The concentrations of
cyclophilin mRNA (picograms
mRNA per microgram total
RNA) remained essentially unchanged in both sexes during the same period of time when
proGnRH mRNA levels were increasing. These results provide evidence for postnatal sex-related increases in the levels of
proGnRH mRNA in the rat POA-AH, which are likely to reflect differential regulation by gonadal
steroids.