Male red deer calves, whose mothers had been kept for the last 14 weeks of gestation in long days (18 h light:6 h dark) (group L, n = 7) or short days (6 h light:18 h dark) (group S, n = 5), were kept in constant intermediate daylength (12 h light:12 h dark) from birth to 75 weeks of age. Both groups showed the same live-weight gain. Mean plasma LH concentrations were higher in group L than in group S from birth to 20 weeks of age (averaging 1.55 versus 0.48 ng ml⁻¹, P< 0.001), from 21 to 45 weeks (1.65 versus 1.32 ng ml⁻¹, P < 0.05) and from 46 to 50 weeks (1.84 versus 1.27 ng ml⁻¹, P < 0.001); thereafter, there was no significant difference between the groups (1.81 ng ml⁻¹). Mean concentration of plasma testosterone was relatively low from birth to 30 weeks (averaging 0.38 and 0.27 ng ml⁻¹ (P<0.05) in groups L and S, respectively), but thereafter increased to a maximum which was greater (2.78 versus 1.46 ng ml⁻¹, P < 0.01), and occurred earlier (47 versus 68 weeks of age, P < 0.001) and at lower body weight (82 versus 96 kg, P < 0.01) in group L compared with group S. Growth of antlers started in both groups at 25 weeks, but they hardened earlier in group L than in group S (42 versus 47 weeks of age, P< 0.05). These results provide evidence that in male red deer postnatal photoperiodic change is not required to trigger puberty, that prenatal photoperiodic history influences postnatal reproductive development and that the timing of reproductive maturation in deer raised on 12 h light:12 h dark is advanced by long days experienced prenatally.

Summary. Plasma prolactin concentrations were higher (P < 0·001) in newborn red deer calves whose mothers had been maintained for the last 14 weeks of gestation in long days (18 h light) (group L, n = 9) than in those whose mothers had been kept over the same period in short days (6 h light) (group S, n = 5). After transfer of all hinds and suckled calves on the day of birth to constant intermediate daylength (12 h light), prolactin concentrations decreased exponentially (P < 0·001) in group L calves, but not in group S, during the first 21 days. Thereafter, prolactin fell to a nadir in group L calves and rose to peak values in group S calves at 8–12 weeks post partum (P = 0·003), before converging again by 14 weeks. The pattern of prolactin secretion over the first 14 weeks of life was therefore significantly affected by prenatal photoperiod.

Plasma prolactin concentrations in the adult hinds were higher (P < 0·001) in group L than group S at 4–10 weeks before parturition; they were similarly high around parturition and fell thereafter to baseline values after 7 weeks.

These results provide evidence that deer fetuses respond to photoperiodic information, thereby acquiring a photoperiodic history in utero that influences postnatal responses to photoperiod.

Keywords: prolactin; gestation; photoperiod; deer

Spermatogonial stem cells (SSCs) maintain spermatogenesis throughout the reproductive life of mammals. While A_single spermatogonia comprise the rodent SSC pool, the identity of the stem cell pool in the primate spermatogenic lineage is not well established. The prevailing model is that primate spermatogenesis arises from A_dark and A_pale spermatogonia, which are considered to represent reserve and active stem cells respectively. However, there is limited information about how the A_dark and A_pale descriptions of nuclear morphology correlate with the clonal (A_single, A_paired, and A_aligned), molecular (e.g. GFRα1 (GFRA1) and PLZF), and functional (SSC transplantation) descriptions of rodent SSCs. Thus, there is a need to investigate primate SSCs using criteria, tools, and approaches that have been used to investigate rodent SSCs over the past two decades. SSCs have potential clinical application for treating some cases of male infertility, providing impetus for characterizing and learning to manipulate these adult tissue stem cells in primates (nonhuman and human). This review recounts the development of a xenotransplant assay for functional identification of primate SSCs and progress dissecting the molecular and clonal characteristics of the primate spermatogenic lineage. These observations highlight the similarities and potential differences between rodents and primates regarding the SSC pool and the kinetics of spermatogonial self-renewal and clonal expansion. With new tools and reagents for studying primate spermatogonia, the field is poised to develop and test new hypotheses about the biology and regenerative capacity of primate SSCs.

Ovariectomized, oestradiol-implanted Soay ewe lambs from 21 September (aged 21 weeks) had restricted (liveweight maintenance) (n = 4) or unrestricted food (n = 4); ovary-intact lambs had unrestricted food (n = 8). LH activation in ovariectomized lambs on restricted and unrestricted food and onset of ovulatory cycles in ovary-intact lambs all occurred on 7 December (sed 8.8 days) (32 weeks), but at different liveweights (24.2, 17.9 and 18.3 kg, respectively, sed 1.22). LH pulse frequency was similar in ovariectomized lambs on restricted and unrestricted food. From 29 August (aged 18 weeks), Soay ewe lambs in seasonally advanced decreased artificial daylength were given restricted food, unrestricted food, or food was restricted for 8 weeks and then unrestricted (n = 8 per group). Ovarian cycles started 3 weeks earlier than in lambs in natural photoperiod on similar dates for all three groups (14, 18 and 19 November, respectively, sed 5.5 days) (29 weeks), but at different liveweights (16.2, 20.7, and 18.4 kg, respectively, sed 0.87). From 1 August, Suffolk × Greyface ewe lambs (aged 16 weeks) had restricted food, unrestricted food, or food restricted for 8 weeks and then unrestricted (n = 8 per group). By 1 November (29 weeks), 0/8 lambs on restricted food (29.3 ± 0.92 kg) but 8/8 lambs on unrestricted food and 5/8 lambs on 8 weeks of restricted food had ovulated (mean dates: 16 October ± 2.5 days (27 weeks, 40.1 ± 1.02 kg), and 1 November ±3.0 days (29 weeks, 35.5 ± 1.23 kg), respectively. Thus, nutritional growth restriction during the 11 weeks preceding normal puberty delayed pubertal date in the improved breed but did not influence the timing of puberty in the unimproved Soay breed within the weight range studied.

Epidemiological and animal studies strongly indicate that the environment experienced in utero determines, in part, an individual’s likelihood of developing cardiovascular disease in later life. This risk has been further linked to impaired kidney function, as a result of compromised development during fetal life. The present study therefore examined the influence of maternal nutrient restriction (NR), targeted at specific periods of kidney development during early to mid gestation, on the mRNA abundance of receptors for glucocorticoid (GCR), growth hormone (GHR) and insulin-like growth factors-I (IGF-IR) and -II (IGF-IIR), and the IGF-I and -II ligands. This was undertaken in both singleton and twin fetuses. At conception ewes were randomly allocated to either an adequately fed control group or one of four nutrient-restricted groups that were fed half the control amount from 0 to 30, 31 to 65, 66 to110 or 0 to110 days gestation. At 110 days gestation all ewes were humanely euthanased and fetal kidneys and surrounding adipose tissue sampled. There was no effect of NR or fetal number on kidney weight, shape or nephron number, but the surrounding fat mass was increased in singleton fetuses exposed to NR for 110 days. An increase in kidney mRNA abundance with NR only occurred in singleton fetuses where IGF-IR mRNA was enhanced with NR from 66–110 days gestation. In twin fetuses, NR had no effect on mRNA abundance. However, for all genes examined mRNA expression was lower in the kidneys of twin compared with singleton fetuses following NR, and the magnitude of the effect was dependent on the timing of NR. In conclusion, the abundance of mRNA for receptors which regulate fetal kidney development are lower in twin animals compared with singletons following periods of nutrient deficiency. This may impact on later kidney development and function.

This study aimed to determine whether reduced fetal ovary folliculogenesis in ewes undernourished during early/midpregnancy is associated with altered ovarian cell proliferation and/or the expression of apoptosis-regulating genes. Groups of ewes (n = 11–19) were fed either 100% (high; H) or 50% (low; L) of metabolisable energy requirements for live-weight maintenance during selected windows of gestation. All animals were killed at days 50, 65 or 110 of gestation. Between mating and slaughter, control animals were fed the H ration, while animals of other subgroups were fed the L ration from (a) mating to slaughter at 50, 65 or 110 days; (b) 0 to 30 days; (c) 31 to 50 or 65 days; or (d), in the day 110 slaughter group only, from 66 to 110 days. Bouin’s-fixed fetal ovaries were examined for (a) Ki67 immunoexpression (proliferation) and (b) Bax and Mcl-1 (apoptosis-regulating genes) expression by in situ hybridisation (day 110) and immunohistochemistry (days 50, 65 and 110). At day 50, maternal nutrition had no effect on Ki67, predominant in germ cells, or Bax and Mcl-1, predominant in the oocytes. Restricted maternal food intake from 0 to 30 days significantly reduced staining for Ki67 in germ cells at day 65 (P < 0.05) but increased staining in granulosa cells at day 110 (P < 0.05). In animals fed the L ration for 110 days, primordial follicle Bax and Mcl-1 were significantly increased (Bax: P < 0.01; Mcl-1: P < 0.05). Granulosa cell Bax was also increased (P < 0.05). When the L ration was fed from 66 to 110 days, granulosa cell Bax (P < 0.05) and primordial follicle Mcl-1 (P < 0.01) were also significantly increased. In the fetal ovarian vasculature, animals underfed for 0–110 days had significantly elevated perivascular Mcl-1 (P < 0.001) and endothelial Bax expression (P < 0.05). Moreover, at day 110, endothelial Mcl-1 was increased by underfeeding from 0 to 30 days (P < 0.05). These data indicate that maternal undernutrition alters proliferation and the expression of apoptosis-regulating genes in the developing fetal ovary. The precise mechanism depends on the window of maternal food restriction.