Records representing data from 1,500 barren Holstein cows over an 8-yr period from a large commercial dairy farm in northern Mexico were analyzed to determine the effects of lactation number and season and year of initiation of lactation on milk production of cows induced hormonally into lactation and treated with recombinant bovine somatotropin (rbST) throughout lactation. Peak and 305-d milk yields were also assessed as predictors of total milk yield in cows induced into lactation. A significant quadratic relationship was found between 305-d milk yield and number of lactation [7,607±145 and 9,548±181 kg for first- and ≥6-lactation cows, respectively; mean ± standard error of the mean (SEM)] with the highest production occurring in the fifth lactation. Total milk yields of cows with ≤2 lactations were approximately 4,500 kg less than milk yields of adult cows (the overall average ± standard milk yield was 13,544±5,491 kg per lactation and the average lactation length was 454±154 d). Moreover, 305-d milk production was depressed in cows induced into lactation in spring (8,804±153 kg; mean ± SEM) and summer (8,724±163 kg) than in fall (9,079±151 kg) and winter (9,085±143 kg). Partial regression coefficients for 305-d milk yield and peak milk yield indicated an increment of 157 kg of milk per lactation per 1-kg increase in peak milk yield (r(2)=0.69). Neither peak milk yield (r(2)=0.18) nor 305-d milk yield (r(2)=0.29) was accurate for predicting total milk yield per lactation. Year, parity, and season effects had significant influence on milk yield of cows induced into lactation and treated with rbST throughout lactation, and peak milk yield can assist in the prediction of 305-d milk yield but not total milk yield. This study also showed that hormonal induction of lactation in barren high-yielding cows is a reliable, practical, and affordable technique in countries where rbST treatment and prolonged steroid administration of dairy cows are legally permitted.

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Establishment of the hypothalamic-hypophyseal-gonadal function is dependent on the highly controlled and dynamic interactions between regulatory signals from the brain, pituitary and gonads, all of them leading to the attainment of reproductive capacity, where a coordinated and timely activation of GnRH neurons must occur. The GnRH neurons extend their neurosecretory axons to the hypothalamus where GnRH is released into the pituitary portal vessels to elicit the secretion of LH and FSH, which in turn, will promote gonadal development and support reproductive physiology. Genetic studies have demonstrated that disabling mutations and targeted deletions of the G-protein-coupled receptor (GPR54) generated hypogonadotropic hypogonadism. This link between GPR54 and reproduction, generated attention to the natural ligands of the GPR54 receptor, known as kisspeptins, which are translational products of the hypothalamic gene KiSS1. Recent advances in kisspeptin research have defined a major role of this molecule in controlling the onset of the reproductive function observed at puberty. The aim of this review is to highlight the basic endocrine and genetic concepts involved in the establishment of the hypothalamic-hypophyseal-gonadal axis function which promotes the onset of the reproductive function during puberty. The review highlights what is currently known about the kisspeptin-GPR54 signalling system in the activation of the GnRH neurons.

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