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The objectives of the present study were to quantify the effects of a biological chronic stressor (lameness) on the duration and frequency of different oestrous behaviours in parallel with milk hormone profiles. Dairy cows 51.8 +/- 1.4 days postpartum (n = 59), including 18 non-lame control cows, were scored for lameness and closely observed for signs of oestrus having had their follicular phases synchronized by administration of gonadotrophin-releasing-hormone (GnRH) followed by prostaglandin F(2alpha) (PG) 7 days later. Lameness shortened the period when herd-mates attempted to mount the lame cows (1.83 +/- 0.69 h vs 5.20 +/- 1.53 h; p = 0.042) but did not affect the overall duration of total behaviours (lame 12.3 +/- 1.3 h vs non-lame 15.2 +/- 1.3 h). Lameness also lowered the intensity of oestrus [1417 +/- 206 points (n = 18) vs 2260 +/- 307 points (n = 15); p = 0.029]. Throughout the synchronized oestrous period, lame cows mounted the rear of herd-mates less frequently (p = 0.020) and tended to chin rest less (p = 0.075). Around the period of maximum oestrous intensity, lameness also diminished the proportion of cows mounting the rear of another cow and chin resting (p = 0.048, p = 0.037, respectively). Furthermore, lame cows had lower progesterone values during the 6 days before oestrous (p < or = 0.05). Fewer lame cows were observed in oestrus following PG (non-lame 83%, lame 53%; p = 0.030); however, if prior progesterone concentrations were elevated, lame cows were just as likely to be observed in oestrus. In conclusion, following endogenous progesterone exposure, lameness shortens the period when herd-mates attempt to mount lame cows but does not affect the incidence of oestrous. However, lame cows are mounted less frequently and express oestrus of lower intensity. This is associated with lower progesterone prior to oestrus but not with abnormal oestradiol or cortisol profiles in daily milk samples.

The present study investigates the influence of alpha(1)-adrenoreceptors in GnRH release in vitro and determines whether oestradiol modulates alpha(1)-adrenoreceptor-GnRH interaction. Within 10 min after ewe sacrifice, saggital midline hypothalamic slices were dissected, placed in oxygenated Minimum Essential Media-alpha (MEM-alpha) at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without oestradiol (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to specific alpha(1)-adrenoreceptor agonist (methoxamine) or antagonist (thymoxamine) at various doses (0.1-10 mm). The alpha(1)-adrenoreceptor agonist (10 mm) increased (p < 0.05) GnRH release at 90 min both in presence and absence of oestradiol. However, in presence of oestradiol, alpha(1)-adrenoreceptor agonist (10 mm)-induced GnRH release remained elevated (p < 0.05) for at least 60 min. The bioactivity of the released GnRH was studied using a hypothalamus-pituitary sequential double-chamber perifusion. Only after exposure of hypothalamic slices to alpha(1)-adrenoreceptor agonist (10 mm), did the hypothalamic eluate stimulate LH release from pituitary fragments (n = 9, 7.8 +/- 12.3-36.2 +/- 21.6 ng/ml) confirming that the alpha(1)-adrenoreceptor agonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is under stimulatory noradrenergic control and this is potentiated in the presence of oestradiol.

The present study examines the involvement of GABA(A or B) receptors in gonadotrophin-releasing hormone (GnRH) release in vitro and determines whether oestradiol modulates gamma-aminobutyric acid (GABA)-GnRH interaction. Within 10 min after ewe killing, hypothalamic slices were dissected and placed in oxygenated Minimum Essential Media (MEM)-alpha at 4 degrees C; within 2 h, slices were singly perifused at 37 degrees C with oxygenated MEM-alpha (0.15 ml/min), with or without oestradiol (24 pg/ml). After 4 h equilibration, fractions were collected for 4 h interposed with a 10 min exposure to specific GABA(A or B) receptor ligands (0.1-10 mM). The GABA(A or B) agonists (muscimol or baclofen) did not greatly influence GnRH release. However, GnRH increased (p < 0.05) after exposure to 10 mM GABA(A or B) antagonists (bicuculline or CGP52432, respectively). The GABA(A) antagonist stimulated greater sustained GnRH release (p < 0.05) in the absence of oestradiol than in its presence. The bioactivity of the released GnRH was studied using a hypothalamus-pituitary sequential double-chamber perifusion. Only after exposure of hypothalamic slices to the GABA(A) antagonist, did the hypothalamic eluate stimulate luteinizing hormone release from pituitary fragments (p < 0.05) confirming that the GABA(A) antagonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is predominantly under GABA(A) receptor inhibitory control and this is attenuated in the presence of oestradiol.

The objectives of the present study were to determine if lameness, a model for a natural chronic stressor, affects hormone concentrations in milk prior to estrus and/or the subsequent expression of estrus in the postpartum period. Dairy cows>20 days postpartum were scored for lameness and observed for estrus intensity using a weighted scoring system (>100 points=estrus=Day 0). Increasing lameness score was not associated with daily profiles of milk progesterone (throughout Days -18 to 0), estradiol (Days -6 to 2) or cortisol (Days -18 to 2) around estrus, maximum estradiol values or estradiol concentrations on Day 0. However, post hoc pair wise comparisons revealed that prior to estrus, severely lame cows had lower maximum progesterone concentrations compared to nonlame cows (1.3+/-0.1, 1.2+/-0.2, 0.7+/-0.1 ng/ml milk; P=0.042). Furthermore, severely lame cows expressed behavioral estrus with lower intensity (284+/-128 points, n=9) compared to moderately lame (662+/-310 points, n=9) or nonlame animals (583+/-275 points, n=18; P=0.05 and P=0.02, respectively). Resting concentrations of cortisol (Days 20-80 postpartum) did not vary between days postpartum or lameness score. The incidence of behavioral estrus was not affected by increasing lameness score, as 54.2%, 56.2% and 50.0% periods with low progesterone were associated with spontaneous estrus expression, respectively. Concluding, in this biological model of chronic stress, lameness did not affect the incidence of behavioral estrus but did reduce estrus intensity once ovarian cyclicity had resumed after calving. This reduced intensity of estrus was associated with lower maximum progesterone values prior to estrus but not abnormal daily cortisol or estradiol values in milk.

Contents The aim of this study was to investigate how acute insulin-induced hypoglycaemia (IIH) alters the activity of cells containing oestradiol receptor α (ER α) or somatostatin (SST) in the arcuate nucleus (ARC) and ventromedial nucleus (VMN), and ER α cells in the medial preoptic area (m POA) of intact ewes. Follicular phases were synchronized with progesterone vaginal pessaries. Control animals were killed at 0 h or 31 h (n = 5 and 6, respectively) after progesterone withdrawal (PW; time zero). At 28 h, five other animals received insulin (INS; 4 iu/kg) and were subsequently killed at 31 h. Hypothalamic sections were immunostained for ER α or SST each with c-Fos, a marker of neuronal transcriptional activation. Insulin did not alter the percentage of activated ER α cells in the ARC; however, it appeared visually that two insulin-treated animals (INS responders, with no LH surge) had an increase in the VMN (from 32 to 78%) and a decrease in the m POA (from 40 to 12%) compared to no increase in the two INS non-responders (with an LH surge). The percentage of activated SST cells in the ARC was greater in all four insulin-treated animals (from 10 to 60%), whereas it was visually estimated that activated SST cells in the VMN increased only in the two insulin responders (from 10 to 70%). From these results, we suggest that IIH stimulates SST activation in the ARC as part of the glucose-sensing mechanism but ER α activation is unaffected in this region. We present evidence to support a hypothesis that disruption of the GnRH/LH surge may occur in insulin responders via a mechanism that involves, at least in part, SST cell activation in the VMN along with decreased ER α cell activation in the m POA. [ABSTRACT FROM AUTHOR]