89 Does progesterone block the nerve growth factor–induced luteinizing hormone surge in llamas?

Abstract

The central inhibitory effects of progesterone on gonadotrophin secretion have been well documented in several species, including camelids. Nerve growth factor (NGF) in seminal plasma triggers ovulation in camelids and is thought to act at the level of the hypothalamus. The objective of the study was to determine the effect of progesterone on NGF-induced LH release in llamas. In Experiment 1, llamas were assigned to a low, medium, or high progesterone group (n = 4 per group). The low progesterone group consisted of non-mated (non-ovulatory) llamas, the medium progesterone group consisted of mated llamas (luteal phase; 3–4 weeks pregnant), and the high progesterone group consisted of non-mated llamas given a single intramuscular (IM) dose of progesterone (300 mg IM, Progesterone BioRelease LA). A jugular catheter was placed, and the following day llamas were given an intravenous dose of 1 mg of NGF isolated from seminal plasma. Blood samples were taken every 30 min from 1 h before to 5.5 h after NGF treatment. In Experiment 2, the pituitary LH response to gonadotrophin-releasing hormone (GnRH) was compared between llamas treated with either Progesterone BioRelease LA or saline (n = 4 per group). Sixteen hours later, llamas in both groups were given 50 µg of gonadorelin (GnRH) IV, and blood samples were collected by jugular puncture at 0.5 h before and 0, 1, 2, and 4 h after GnRH. Blood samples were centrifuged, and plasma was stored frozen until radioimmunoassay for LH and progesterone. Data are presented as mean ± s.e.m. Data were analysed by one-way ANOVA for single-point and repeated-measures, and independent or paired t-tests. In Experiment 1, plasma progesterone concentrations in the low, medium, and high progesterone groups were 0.6 ± 0.3, 8.2 ± 0.4, and 14.9 ± 1.2 ng mL⁻¹, respectively, at the time of NGF treatment (P < 0.05). Circulating concentrations of LH did not differ among progesterone groups (treatment, P = 0.49; time, P < 0.01; treatment × time interaction, P = 0.65). In all groups, LH concentrations were elevated within 30 min of NGF administration, reached a peak by 2 h, and remained elevated beyond the sampling period. Comparison of samples collected during the pretreatment period (i.e. −60, −30, and 0 min), however, revealed that plasma LH concentrations in the high progesterone group were half that of the low and medium progesterone groups (P < 0.03). In Experiment 2, plasma progesterone concentrations in the progesterone- and saline-treated groups were 12.7 ± 2.2 and 1.3 ± 0.3 ng mL⁻¹, respectively (P < 0.01). Despite the difference in circulating progesterone concentrations, the LH response to GnRH treatment was not different between groups (treatment group, P = 0.43; time, P < 0.01; treatment × time interaction, P = 0.84). Results demonstrate a suppressive effect of progesterone on basal LH release in llamas, but no suppressive effect on NGF- or GnRH-induced surge release from the pituitary gland. Results are consistent with the hypothesis that the site of action of NGF is downstream of the hypothalamic site of action of progesterone.

This research was supported by NSERC Canada.