Marongiu, Maria Laura and Gulinati, Alessandro (2008) Opioid inhibition of the pulsatile luteinizing hormone release as assessed by naloxone treatment in the lactating rabbit. In: 9th World rabbit congress: proceedings, June 10-13, 2008, Verona, Italy. Brescia, Fondazione iniziative zooprofilattiche. p. 387-391. (Fondazione iniziative zooprofilattiche e zootecniche, 72). ISBN 9788890281464. Conference or Workshop Item.
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Since in nursing rabbits sexual receptivity and fertility achieved after AI appear to be depressed during lactation, the effect of endogenous opioid peptides (EOP) on serum LH were investigated in lactating rabbits (n=30) by administration of the opiate antagonist naloxone (nal). Blood samples were collected every 15 min for 4 h via an indwelling catheter inserted in the central ear artery. After the first h of sampling, the rabbits received i.v. saline (SAL, n=10); nal (LN, 0.5 mg/kg, n=10); or nal (HN, 1.0 mg/kg, n=10). The pulsar algorithmic procedure for the study of pulsatile hormone secretion was used to calculate mean and basal LH concentrations, frequency and amplitude of LH pulses. Data from the statistical analysis are presented as mean ± SE of area under the curve (AUC) units of LH response. Mean LH concentration during the 60 min pre-challenge period was 0.24±0.03 ng/ml. The AUC of LH during that period did not differ among treatment groups (LN=16.6±4.1, HN=11.8±2.9 and SAL=14.3±4.0 area units). In the SAL group LH secretion remained low during the 4 h sampling period. Mean and basal LH concentrations were 0.21±0.05 ng/ml and 0.03±0.02 ng/ml (LN=0.59±0.13 ng/ml and 0.20±0.04 ng/ml; HN=0.38±0.09 ng/ml and 0.13±0.03 ng/ml). The mean pulse peak was 0.70±0.15 ng/ml (LN=1.95±0.37 ng/ml; HN=1.26±0.23 ng/ml), and the mean pulse amplitude was 0.67±0.14 ng/ml (LN=1.89±0.36 ng/ml; HN=1.22±0.21 ng/ml). A lower number of pulses (1.88±0.35) was also detected for the 4 h period (LN=2.57±1.13; HN=2.34±1.11). Nal treatment increased LH release. A greater AUC was observed during the 60 min post nal period in both nal-treated groups (LN=55.0±15.5 and HN=38.8±10.3 vs. SAL=5.9±2.7 area units; P <0.01). Rabbits receiving 0.5 mg/kg nal had an increased (P <0.05) AUC (LN=105.9±26.1 area units) through 180 min after nal administration compared with the saline-treated group (SAL=34.9±9.2 area units). The group LN differed from the SAL group through the 180 min post-nal period, while the HN group differed only for 60 min. Nal-treated groups (LN and HN) did not differ in either of the post-nal periods (60 and 180 min). Since all the experimental rabbits presented a clear LH surge after the nal challenge, the suppression of pituitary LH release has been shown to be associated with EOP activity. EOP may have modulated hypothalamic secretion of GnRH, resulting in a tonic inhibition of LH secretion. However, further studies are necessary to better clarify EOP-cortisol interaction in the lactating rabbit doe at the moment of AI and after an i.m. injection of a GnRH analogue to induce ovulation.
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