The gonadal steroids can influence both brain function and organization. Organizational effects of the gonadal steroids are determined during a critical period of development (although the manifestation of their effect may not be evident until adulthood); the nascent steroid need not be present for the effect to be preserved. In contrast, activational effects require the presence of the steroid, and are terminated when the steroid is removed. Both classes of steroid effect have been observed in regions of the brain that play a role in the reproductive process. In one of these, the preoptic area (POA), axons containing an opiate peptide, metenkephalin, (m-ENK), in the periventricular region of the POA (pePOA) show sex differences in density, and the m-ENK fiber pattern can be manipulated by alteration of the gonadal steroids. Preliminary studies indicate that this peptide system shows both organizational and activational effects of steroids. This proposal is designed to further examine the sexual dimorphism of the m-ENK system. Specifically, experiments will be designed to: 1) Characterize the anatomical organization of the sexually dimorphic pePOA and its m-ENK fiber system at light microscopic and ultrastructural levels by examining the organization of pePOA and its m-ENK fiber distribution at the light microscopic (LM) and ultrastructural (EM) levels, 2) determine the degree to which the expression of this sexually dimorphic patterna in m-ENK immunoreactivity is determined by activational actions of gonadal steroids by exploring the changes in m-ENK immunoreactivity produced by gonadal steroids, the time course of this effect, and the selectivity of this activational process for different steroids, and 3) determine the degree to which the expression of this sexually dimorphic pattern in m-ENK immunoreactivity and neuronal density is determined by organizational actions of gonadal steroids by exploring the effects of gonadal steroids administered during the neonatal period on the sexually dimorphic patterns of the pePOA.

R01NS023591

1986-04-01

1989-03-31