Primer pheromones elicit slow, long-lasting changes in physiology and behavior, due in part to pheromone-mediated regulation of gene expression in the brain. In contrast, releaser pheromones elicit rapid behavioral responses, and so are not expected to also cause changes in brain gene expression. We tested this prediction by exposing honey bees to isopentyl acetate (IPA), a major component of the sting alarm pheromone which alerts bees to danger and provokes rapid defensive behavior. In laboratory experiments, repeated exposure to IPA led to a decrease in responsiveness, suggesting a long-lasting change in behavior in response to this releaser pheromone. The brain’s genomic response was then studied by analyzing the level of the immediate early gene c-Jun, one of the transcription factors initiating changes in gene expression. Exposure to IPA caused an increase in the expression of c-Jun in the antennal lobes. This induction of gene expression, previously assumed to be characteristic of primer pheromones, gives new insights into the mechanisms by which releaser pheromones can affect animal behavior and may lead to some reconsideration about the distinction between these two groups of pheromones.