Impact of pre- and Post-Natal Nutritional Extremes on Responsiveness of Ovariectomized, Sexually Mature Heifers to a Neurokinin B Agonist During Progesterone Dominance.

Objectives were to test the hypothesis that nutritional extremes during prenatal development interact with postnatal nutrition during the juvenile period of heifers to impact KNDy neuron responsiveness to a neurokinin B (NKB) agonist (Senktide) during progesterone dominance. Heifers were selected from a larger population programmed nutritionally using a 3x2 factorial arrangement of pre- and post-natal diets. Bos indicus-influenced cows (n = 95) were fed to achieve body condition scores (BCS; 1-9 scale) of 3-3.5 (L; thin), 5.5-6 (M; moderate), or 7.5-8 (H; obese) by the onset of the third trimester and maintained thereafter. Heifer offspring were weaned at 3-3.5 mo of age and assigned to either a low-(L; 0.5 kg/day) or high-gain (H; 1 kg/day) diet until 8 mo of age, then fed a common diet until puberty. For the current experiment, heifers (n = 18; 6/group) representing LL, MH, and HH combinations were ovariectomized postpubertally (17.1 mo of age) and received estradiol (E2) replacement to maintain basal E2 concentrations at 2-4 pg/mL. To achieve progesterone dominance, 3 CIDR devices were placed intravaginally 6 days prior to the initiation of Senktide challenge. Heifers were sampled for a 4.5-h period and received intravenous injections of saline or Senktide (14.8 ug/kg I.V.) at 0, 90, and 180 min. Jugular blood samples were collected at 10-min intervals for radioimmunoassay of LH. Irrespective of Senktide treatment, heifers in the MH group had greater pulse amplitudes (P = 0.016) and mean concentrations (P < 0.0001) of LH compared with both the HH and LL groups. Senktide treatment increased (P = 0.003) concentrations of LH compared with saline in all groups; however, the response to Senktide was greatest in the MH group compared with HH and LL. Pre- and postnatal nutritional extremes appear to interact to impact KNDy neuron responsiveness to NKB receptor signaling in heifers. [ABSTRACT FROM AUTHOR]