Stress is a known inhibitor of reproductive function. The mechanisms by which stress acts to influence the reproductive axis have been intensely studied and appear to be extremely varied. Gonadotropin-releasing hormone (GnRH) is a critical component of the vertebrate reproductive axis and directly causes pituitary gonadotropin synthesis and release. A second neuropeptide, gonadotropin-inhibitory hormone (GnIH), directly inhibits pituitary gonadotropin synthesis and release in birds. We hypothesized that stress effects upon reproduction are mediated via the hypothalamic GnIH system. We examined the effects of capture-handling stress in the hypothalamus of male and female adult house sparrows (Passer domesticus) at the start (spring) and end of the breeding season (fall). We quantified numbers of GnIH neurons to provide an estimate of hypothalamic GnIH content. In addition, we quantified the expression of the protein product of the immediate-early gene, EGR-1, using this as an indicator of neuronal activation. We saw an increase in EGR-1 positive cells in the paraventricular nuclei of stressed birds as opposed to controls at both collecting times, but this stress response was more apparent in the spring as opposed to the fall. There were more GnIH-positive neurons in fall birds versus those sampled in the spring, and a significant increase in GnIH positive neurons was seen in stressed birds only in spring. GnIH cells show little to no activation of EGR-1, suggesting that EGR-1 is not involved in GnIH transcription in response to capture-handling stress. These data imply an influence of stress upon the paraventricular nucleus and the GnIH system that changes over the annual cycle of reproduction.