Rats exposed to progesterone in the womb were better at getting away from unpleasant stimuli, a task called active avoidance, but performed worse in mazes. Hull knew that normally male rats were better at mazes, a task requiring a sense of absolute direction, and worse at learning active avoidance. Normally, testosterone produced by male fetuses and neonates masculinizes their brains and genitals. The progesterone Hull administered apparently had interfered with testosterone's masculinizing effects. This finding presented another question.
All neurons use neurotransmitters for communication.
Knowing that L-Dopa treatment for Parkinson's disease frequently increased libido and sexual potency of male patients, dopamine seemed like a reasonable candidate to target. To her surprise, the dopamine antagonist made male rats less male no matter when it was administered, and testosterone levels weren't affected. It was a defining moment. To my knowledge, this was the first report of demasculinization by drugs that don't affect steroid hormones either directly or indirectly. The respected journal Science published the research results in 1984, but the discovery had little impact on the field.