In adult male rats, serum luteinizing hormone (LH) rises within a few hours of castration. By contrast, in adult female rats, serum LH does not increase reliably until 4–6 d after ovariectomy. The release of gonadotropin-releasing hormone (GnRH) declines in female rats postovariectomy, suggesting an increase in inhibition of the release of GnRH. We investigated whether differences in γ-aminobutyric acid (GABA)-ergic transmission, which inhibits GnRH release, accounts for the sex difference in the response of serum LH to gonadectomy. We examined the effects of GABA-A receptor antagonist bicuculline methiodide (BMI), GABA-B receptor antagonist phaclofen, and transaminase inhibitor aminooxyacetic acid (AOAA), injected subcutaneously, on the postgonadectomy rise in LH. AOAA prevented the postcastration rise in male rats (p<0.05). Female rats treated with BMI, phaclofen, or both BMI and phaclofen (p<0.05) showed a significant increase in LH postovariectomy. BMI had no effect in male rats. GnRH antagonist blocked the BMI-induced increase in serum LH. We conclude that the delay in the rise of serum LH in female rats postovariectomy is at least partly owing to GABAergic inhibition of the release of GnRH.