Absence of Brain Opioid Peptide Modulation of Luteinizing Hormone Secretion in the Prepubertal Gilt1

Three experiments were conducted to evaluate the role of endogenous opioid peptides (EOP) in modulating luteinizing hormone (LH) secretion in the prepubertal gilt. In Experiment I, 8 prepubertal (P) gilts, 160–170 days of age (puberty = 197 ± 10 days), received either 1 (n=2), 3 (n=3), or 6 (n=3) mg/kg BW of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected by jugular vein cannula every 15 min for 2 h before and 2 h after NAL. All doses of NAL failed to alter serum LH concentrations. In Experiment II, 21 P gilts 160–170 days of age and 21 mature (M) gilts were ovariectomized (OVX). At the time of OVX, gilts were classified as prepubertal if their ovaries were devoid of corpora albicantia and corpora lutea. Three weeks after OVX, P and M gilts were injected twice daily for 10 days with either 0.85 mg/kg BW of progesterone (P4) or oil vehicle (V), resulting in the following groups: PP4 (n=11), PV (n=10), MP4 (n=11), and MV (n=10). All gilts received 1 mg/kg BW of NAL on the last day of treatment. Blood samples were collected via a jugular cannula every 15 min for 4 h before and 2 h after NAL treatment. NAL treatment resulted in an increase (p<0.05) in serum LH concentrations only in the MP4 gilts. In Experiment III, 15 OVX gilts 280 days of age were used. Ten of the 15 gilts were OVX prior to puberty at 160 days of age and were classified as chronologically mature (CM) at the time of treatment. The remaining 5 gilts were OVX after puberty, and were classified as sexually mature (SM) at the time of treatment. An additional 5 gilts were OVX prior to puberty at 160 days of age and were 170 days of age at the time of the experiment. Gilts were classified P as described in Experiment II. All pigs were injected with P4 as described in Experiment II. Four days prior to the start of 1 i s treatment, 5 CM gilts were injected with 10 µg/BW of estradio1–17P (E2), resulting in the following groups: SMP4 (n=5), CMP4 (n=5), CME2P4 (n=5), and PP4 (n=5). All pigs received 1 mg/kg BW of NAL in saline i.v. on the last day of treatment. Blood was collected as described in Experiment II. In Experiment III, NAL increased (p<0.05) LH secretion in the SMP4, CMP4, and CME2P4 but failed to alter serum LH concentrations in the PP4 gilts. These data suggest that development of EOP modulation of LH secretion is a brain maturational process independent of the ovary in the P gilt.