Manipulation of testosterone in the neonatal rat and pheromonal emission in the adult.
The question we addressed is why the male rat fails to emit the maternal pheromone when caring for young or when injected with prolactin. Our hypothesis was that exposure to androgen neonatally decreases the prolactin sensitivity of the male liver, making that liver incapable of secreting sufficient cholic acid for pheromonal synthesis. Accordingly, we castrated male rats prior to 2 hr of age and injected female rats with testosterone propionate within 8 days of age. Only those animals that had been spared exposure to androgen neonatally showed evidence of the pheromone when injected with prolactin as adults. Moreover, these same animals exhibited a higher output of cholic acid per g liver than their control counterparts (sham-operated males and vehicle-injected females). We conclude that the sex-related capacity for pheromonal emission is differentiated perinatally and involves the sensitivity of the liver to prolactin and its consequent secretion of cholic acid.
D000818:Animals; D000831:Animals, Newborn; D002369:Castration; D002793:Cholic Acids / Q000378:metabolism; D005260:Female; D008099:Liver / Q000378:metabolism; D008297:Male; D008425:Maternal Behavior; D010675:Pheromones / Q000378:metabolism*; D011388:Prolactin / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D012733:Sex Differentiation; D013739:Testosterone / Q000502:physiology*
D002793:Cholic Acids; D010675:Pheromones; D013739:Testosterone; D011388:Prolactin