The onset of puberty in mammals involves an increase in the pulsatile release of GNRH and LH. The KISS1 gene is essential for pubertal development, and its product, kisspeptin, stimulates the release of LH. The objective of this study was to determine the effects of kisspeptin in the hypothalamic-adenohypophyseal-gonadal axis of prepubertal ewe lambs. Ewe lambs (28 weeks of age) were treated intravenously with saline (control, nZ6) or kisspeptin (20 mg kisspeptin; nZ6) every hour for 24 h. Kisspeptin stimulated pulse-like release of LH within 15 min following injections, and increased the frequency and amplitude of LH pulses, and mean circulating concentrations of LH and estradiol. A surge-like release of LH was observed in four kisspeptin-treated lambs beginning 17 h after the onset of treatment, and all four lambs had elevated circulating concentrations of progesterone within 5 days post-treatment. However, circulating concentrations of progesterone decreased within 2 days after the initial rise in three of the four ewe lambs, indicating that induced luteal activity was of short duration. The proportion of lambs that were pubertal (defined by circulating concentrations of progesterone above 1 ng/ml for at least 7 days) by 35 weeks of age (8/11) and the mean age at puberty (32G1 weeks) for those reaching puberty within the experimental period did not differ between treatments. Results support a role for kisspeptin in the activation of the hypothalamic-adenohypophyseal axis leading to the onset of puberty in ewe lambs.

Onset of puberty is characterised by a marked increase in the frequency of release of gonadotrophin-releasing hormone (GnRH) and luteinising hormone (LH). The Kiss1 gene plays a critical role in pubertal development, and its product, kisspeptin, stimulates GnRH and LH release. In the present study, we tested the hypothesis that Kiss1 gene expression in the preoptic area (POA) and hypothalamus increases during maturation of the reproductive neuroendocrine axis in association with increased LH pulsatility. Ovariectomised, oestradiol-replaced lambs were euthanised at 25, 30 and 35 weeks of age. Blood samples were collected before euthanasia to characterise the pattern of LH release. Kiss1 mRNA was detected in coronal sections of the POA and hypothalamus and Kiss1-expressing cells were identified on the basis of silver grain density. The mean number of Kiss1-expressing cells in the POA/periventricular (PeV) areas increased from 25 to 30 weeks of age. No further increase at 35 weeks of age was observed, and the changes in Kiss1 expression in the POA/PeV were independent of changes in LH pulse frequency. The mean number of Kiss1-expressing cells in the arcuate (ARC) nucleus did not differ among age groups, although it was greater in the middle ARC of lambs exhibiting increased frequency of LH release. The density of silver grains per cell did not differ among groups in any of the areas studied. The results obtained indicate that the Kiss1 gene is activated in the POA/PeV and ARC of ewe lambs during juvenile development, and that kisspeptin neurones in the middle ARC, in particular, are involved in the acceleration of pulsatile LH release during maturation of the reproductive neuroendocrine axis in ewe lambs.

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Atopic dermatitis and recurrent urticaria are associated with type I IgE-mediated hypersensitivity in humans (Kaplan & Greaves, 2009;Leung, 1999), with evidence to support a similar relationship in horses (Equus caballus) (Rüfenacht et al., 2005;Stepnik et al., 2012).In horses, urticaria is the result of mast cell and basophil degranulation in the skin releasing histamine and other inflammatory mediators causing focal vasculitis (Hinden et al., 2012; Rüfenacht et al., 2005). One method of controlling clinical signs associated with these disorders is via corticosteroid or antihistamine administration.Corticosteroids, particularly dexamethasone and prednisolone, have demonstrated efficacy for controlling inflammation associated with urticaria in horses (Scott and Miller, 2011). However, they are not without risk of severe side effects including laminitis (Bailey, 2010) and immune suppression (Leclere, 2017).Antihistamine receptor antagonists target either H1 or H2 histamine receptors, with the latter primarily aimed at reducing gastric acid production (Furr & Murray, 1989). H1 antagonists interact with histamine receptors located on cells within various tissues (vascular endothelium, bronchial smooth muscle, and peripheral nerve endings) to stop histamine binding and therefore prevent histamine's pro-inflammatory effects (Leurs et al., 2002) that lead to clinical signs. While various H1 antagonists are commonly used in horses, including hydroxyzine,