The aim of the study was to understand why immature 60-day-old gilts produce delayed low amplitude luteinizing hormone (LH) surges in response to oestradiol benzoate. In Expt 1, gilts (n = 36) were challenged with oestradiol benzoate and subsequently received either no further treatment or were infused with saline or various doses of the opioid antagonist, naloxone, for 6-48 h during the expected LH surge (48-96 h after oestradiol benzoate). No differences were observed among groups in the magnitude or duration of the LH surge. In contrast to the other groups, LH concentrations in gilts infused for 48 h with naloxone did not decrease after the surge period. In Expt 2, gilts (n = 34) were challenged with oestradiol benzoate or sesame oil and subsequently received pulses of luteinizing-hormone-releasing hormone (LHRH) or saline solution during the expected surge period. Two other groups were fed methallibure to pharmacologically suppress the oestradiol benzoate-induced LH surge. In addition, one of these groups was given pulses of an LHRH agonist (LHRH-A) during the surge period. Within 2 h of the start of pulsatile LHRH infusion, LH increased in sesame oil-treated gilts, but not in oestradiol benzoate-treated gilts, suggesting that the pituitary responsiveness to LHRH in immature gilts is decreased by oestrogen before the onset of the LH surge. Pulsatile LHRH infusion did not enhance the amplitude of oestradiol benzoate-induced LH surges nor did it advance its onset. Feeding methallibure suppressed the oestradiol benzoate-induced LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)