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Our objective was to determine if prolonged exposure to various durations of light (i.e., photoperiod) would affect serum IGF-I concentrations in heifers. Thus, 16 Holstein heifers, 2 to 4 mo of age, were exposed during a 5-wk pretreatment period to 12 h of cool-white fluorescent light (L) at an intensity of 1200 lux and 12 h of dark (D). At 5 wk, photoperiods were adjusted to 24 L: 0 D (24 L), 20 L: 4 d (20 L), 16 L: 8 D (16 L) or 8 L: 16 D (8 L) per 24 h (n=4 heifers per photoperiod treatment). Blood was sampled at 5 wk and monthly for 4 mo. During each sampling period, blood was collected at 16-h intervals for 48 h and serum IGF-I was determined by RIA. Photoperiod treatment, month of experiment and their interactions affected serum IGF-I concentrations. Averaged over months, concentrations of serum IGF-I was greatest in heifers on 16 L; heifers on 20 L had IGF-I concentrations similar to 8 L, 16 L and 24 L and heifers on 24 L had concentrations similar to that of heifers on 8 L. Heifers in all treatment groups exhibited an increase in serum IGF-I concentration during the 4 mo of treatment. Heifers on 16 L and 20 L exhibited the greatest difference in serum IGF-I concentrations compared with 8L heifers after 3 mo of treatment. In conclusion, 16 L increases concentrations of serum IGF-I above that seen for heifers treated with 8 L or 24 L.

The objective was to determine whether increased energy and protein intake between 2 and 14 wk of age would increase growth rates of heifer calves without fattening. At 2 wk of age, Holstein heifer calves were assigned to 1 of 4 treatments in a 2 x 2 factorial arrangement with 2 levels of protein and energy intake (moderate [M]; high [H]) in period 1 (2 to 8 wk of age) by 2 levels of protein and energy intake (low [L]; high [H]) in period 2 (8 to 14 wk of age) to produce similar initial BW for all 4 treatments. Treatments were ML, MH, HL, and HH, indicating moderate or high energy and protein intake during the first period and low or high intake during the second period. The M diet consisted of a standard milk replacer (21.3% CP, 21.3% fat) fed at 1.1% of BW on a DM basis and a 16.5% CP grain mix fed at restricted intake to promote 400 g of average daily gain (ADG), whereas the L diet consisted only of the grain mix. The H diet consisted of a high-protein milk replacer (30.3% CP, 15.9% fat) fed at 2% of BW on a DM basis and a 21.3% CP grain mix available ad libitum. Calves were weaned gradually from milk replacer by 7 wk and slaughtered at 8 (n = 11) or 14 wk of age (n = 41). In periods 1 and 2, ADG and the gain:feed ratio were greater for calves fed the H diet. Calves fed the H diet were taller after both periods 1 and 2. No difference was observed in carcass composition at 8 wk, but at 14 wk calves fed MH and HH had less water and more fat than calves fed ML and HL. Plasma IGF-I concentrations were greatest for calves fed the H diet during either period. Plasma leptin concentrations were increased in calves fed the H diet during period 1 from 4 to 6 wk of age. Increasing energy and protein intake from 2 to 8 wk and 8 to 14 wk of age increased BW, withers height, and gain:feed ratio. Calves fed the H diet from 8 to 14 wk of age had more body fat than calves fed the L diet. Increased energy and protein intake can increase the rate of body growth of heifer calves and potentially reduce rearing costs.

Serotonin stimulates secretion of growth hormone (GH) in cattle, but the mechanism is unknown. In rats, thyrotropin-releasing hormone (TRH) mediates serotonin-induced secretion of GH. We hypothesized that the same is true in cattle. Cattle were fed for 2h daily to synchronize secretion of GH, such that concentrations of GH were high before and low after feeding. Our first objective was to determine whether or not feeding suppresses serotonin receptor agonist (quipazine) induced secretion of GH. Holstein steers were injected with quipazine (0.2 mg/kg BW) either 1 h before or 1 h after feeding. Quipazine-induced secretion of GH which did not differ in magnitude before and after feeding. If TRH mediates serotonin-induced secretion of GH, then magnitude of TRH-induced secretion of GH should not be different before and after feeding (our second objective). Sixteen meal-fed Holstein steers were injected with 0.3 microg TRH/kg BW either 1 h before or 1 h after feeding. Indeed, magnitude of TRH-induced secretion of GH before and after feeding was not different. Our third objective was to inhibit endogenous TRH with 3,5,3'-triiodothyronine (T(3)) and examine basal, GH-releasing hormone (GHRH)-, TRH- and quipazine-induced secretion of GH. Sixteen Holstein steers were injected daily with either T(3) (3 or 6 microg/kg BW) or vehicle for 20 days and then challenged sequentially with vehicle or GHRH, TRH, or quipazine. T(3) did not affect basal, GHRH- or TRH-induced secretion of GH, but reduced basal secretion of thyroxine. T(3) reduced but did not completely block quipazine-induced secretion of GH. In conclusion, TRH mediates, in part, serotonin-induced secretion of GH in cattle.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a hypothalamic neuropeptide that stimulates release of growth hormone (GH) from cultured bovine anterior pituitary gland cells, but the role of PACAP on the regulation of in vivo secretion of GH in cattle is not known. To test the hypothesis that PACAP induces secretion of GH in cattle, meal-fed Holstein steers were injected with incremental doses of PACAP (0, 0.1, 0.3, 1, 3, and 10 microg/kg BW) before feeding and concentrations of GH in serum were quantified. Compared with saline, injection of 3 and 10 microg PACAP/kg BW increased peak concentrations of GH in serum from 11.2 ng/ml to 23.7 and 21.8 ng/ml, respectively (P0.01). Peak concentrations of GH in serum were similar in steers injected with 3 or 10 microg PACAP/kg BW. Meal-fed Holstein steers were then injected with 3 microg/PACAP/kg BW either 1 hr before feeding or 1 hr after feeding to determine if PACAP-induced secretion of GH was suppressed after feeding. Feeding suppressed basal concentrations of GH in serum. Injection of PACAP before feeding induced greater peak concentrations of GH in serum (19.2 +/- 2.6 vs. 11.7 +/- 2.6 ng/ml) and area under the response curve (391 +/- 47 vs. 255 +/- 52 ng. ml(-1) min) than injection of PACAP after feeding, suggesting somatotropes become refractory to PACAP after feeding similar to that observed by us and others with growth hormone-releasing hormone (GHRH). We concluded that PACAP induces secretion of GH and could play a role in regulating endogenous secretion of GH in cattle, perhaps in concert with GHRH.

The selective dopamine D1 receptor agonist, SKF38393, stimulates release of somatostatin (SS) from perifused bovine hypothalamic slices. Therefore, we hypothesized that SKF38393 activates SS neurons, which, via release of SS, would suppress concentrations of growth hormone (GH) in serum in calves. Our objectives were to determine whether SKF38393: (1) increases the percent of immunoreactive c-Fos protein and Fos-related antigens (Fos/FRA) detected in somatostatin neurons in periventricular (PeVN) and arcuate (ARC) hypothalamic nuclei; (2) reduces concentrations of GH in serum; (3) suppresses growth hormone-releasing hormone (GHRH)-induced release of GH. Meal-fed steers were used to perform these objectives because a synchronous pulse of GH occurs 1-2 hr before feeding in steers allowed access to feed for 2 hr each day. In Experiment 1, two groups of four Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW). Steers were injected i.v. with a lethal dose of sodium pentobarbital 100 min later and their brains were fixed with 4% paraformaldehyde. Dual-label immunohistochemistry was performed on 40 microns free-floating sections using antiserum to SS and to Fos/FRA on sections containing PeVN and ARC nuclei. More SS neurons were detected in the PeVN than in the ARC. The percent of SS neurons with immunoreactive Fos/FRA present was 2.9-fold higher in SKF38393-treated compared with vehicle-injected steers in the PeVN, but was unchanged in the ARC. In Experiment 2, eight Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW) 140 min before meal-feeding. In contrast to controls, concentrations of GH in serum of SKF38393-treated steers did not increase during 140 min before meal-feeding. In Experiment 3, eight Holstein steers were injected s.c. with either vehicle (sterile water) or SKF38393 (5 mg/kg BW), then 100 min later, each steer was injected i.v. with [Leu27,Hse45] bGHRH1-45 lactone (0.2 micrograms/kg BW). Bovine GHRH stimulated release GH into serum in both groups, but concentrations of GH were lower in SKF38393-treated steers. These results show that stimulation of D1 receptors selectively increases activity of SS neurons in the PeVN, and this increased activity is associated with suppressed basal- and GHRH-induced release of GH in serum of meal-fed steers.

Growth hormone-releasing factor is the main endogenous stimulator of somatotropin secretion. Our objective was to compare the effects of recombinant growth hormone-releasing factor and recombinant bST on somatotropin secretion, mammary function, and body composition of lactating, primiparous dairy cows. Cows (118 d of lactation) served as uninfused controls or were infused for 63 d with 12 mg/d of releasing factor or with 29 mg/d of bST. These doses elevated somatotropin in serum to concentrations of similar magnitude. The releasing factor and bST each similarly increased milk yield, yield of milk components, weight of most organs, mobilization of adipose tissue, accretion of lean tissue in the carcass, and metabolic activity (RNA) of mammary tissue. Relative to controls, neither releasing factor nor bST significantly affected cell numbers (DNA) in mammary glands or concentrations of plasmin in milk. None of the variables measured provided evidence for galactopoietic effects of releasing factor independent of somatotropin.

Two experiments were conducted to determine the galactopoietic effects of an analog of growth hormone-releasing factor. Specific replacements were made in the AA sequence of growth hormone-releasing factor to produce a growth hormone-releasing factor analog with enhanced stability in vivo. In Experiment 1, 24 Holstein cows were infused i.v. with 0, .33, 1, or 3 mg/d of growth hormone-releasing factor analog for 20 d. Infusion of the analog increased mean serum concentrations of somatotropin, IGF-I, and NEFA. The analog also increased milk yield as much as 44% relative to that of controls. In Experiment 2, 24 Holstein cows were infused i.v. with 0, .11, .33, or 1 mg/d of analog for 60 d. Infusion of analog increased serum concentrations of somatotropin, IGF-I, and NEFA in a dose-dependent manner. At 1 mg/d, the analog increased SCM yield 28% throughout the infusion period relative to the 0 mg/d controls. In summary, a growth hormone-releasing factor analog increased milk yield and serum concentrations of somatotropin and IGF-I. Furthermore, this galactopoietic activity was mediated through the somatotropic axis.

Effects of activation or blockade of alpha 2-adrenergic receptors on serum growth hormone concentrations were studied in Holstein steers (115 +/- 4 days of age; 112 +/- 4 kg body wt). A pelleted diet was available ad libitum for 2 hr each day. Serum growth hormone concentrations were greater for 80 min immediately before feeding compared with 80 min immediately after removal of feed. Relative to saline-injected controls, activation of alpha 2-adrenergic receptors with clonidine (2 micrograms/kg body wt iv) before feeding rapidly increased serum growth hormone concentrations, but clonidine had no effect when administered after feeding. Compared with vehicle-injected controls, blockade of alpha 2-adrenergic receptors with either idazoxan (20 mg/kg body wt sc) or yohimbine (5 mg/kg body wt sc) decreased serum growth hormone concentrations before as well as after feeding. Feeding abolished the stimulatory alpha 2-adrenergic receptor-mediated increase in growth hormone secretion. Our data support the hypothesis that alpha 2-adrenergic receptor stimulation is an essential event mediating pulsatility of growth hormone secretion before feeding and is required to maintain basal concentrations after feeding.

Eight Holsteins per group received 12 mg/d of recombinant growth hormone-releasing factor or 29 mg/d of recombinant bST or served as untreated controls for 60 d. Milk yield and composition were measured for 10 d before infusion, during infusion (d 0 to 59), and for 20 d after infusion ended. Compared with controls, bST and growth hormone-releasing factor increased SCM during infusion. The SCM yield of cows treated with growth hormone-releasing factor was greater than that of bST-treated cows during the final 20 d of infusion. Relative to controls, bST and growth hormone-releasing factor increased serum concentrations of somatotropin and IGF-I during infusion. Concentrations of somatotropin and IGF-I in serum of bST- and growth hormone-releasing factor-treated cows did not differ during infusion. In summary, growth hormone-releasing factor increased SCM yield more than bST, despite similar serum concentrations of somatotropin and IGF-I. Thus, the galactopoietic action of growth hormone-releasing factor was not explained solely by elevation of total radioimmunoassayable somatotropin and IGF-I in serum.

The objective of this study was to determine if increasing the energy and protein intake of heifer calves would affect growth rates, age at puberty, age at calving, and first lactation milk yield. A second objective was to perform an economic analysis of this feeding program using feed costs, number of nonproductive days, and milk yield data. Holstein heifer calves born at the Michigan State Dairy Cattle Teaching and Research Center were randomly assigned to 1 of 2 dietary treatments (n=40/treatment) that continued from 2 d of age until weaning at 42 d of age. The conventional diet consisted of a standard milk replacer [21.5% crude protein (CP), 21.5% fat] fed at 1.2% of body weight (BW) on a dry matter basis and starter grain (19.9% CP) to attain 0.45 kg of daily gain. The intensive diet consisted of a high-protein milk replacer (30.6% CP, 16.1% fat) fed at 2.1% of BW on a dry matter basis and starter grain (24.3% CP) to achieve 0.68 kg of daily gain. Calves were gradually weaned from milk replacer by decreasing the amount offered for 5 and 12 d before weaning for the conventional and intensive diets, respectively. All calves were completely weaned at 42 d of age and kept in hutches to monitor individual starter consumption in the early postweaning period. Starting from 8 wk of age, heifers on both treatments were fed and managed similarly for the duration of the study. Body weight and skeletal measurements were taken weekly until 8 wk of age, and once every 4 wk thereafter until calving. Calves consuming the intensive diet were heavier, taller, and wider at weaning. The difference in withers height and hip width was carried over into the early post-weaning period, but a BW difference was no longer evident by 12 wk of age. Calves fed the intensive diet were younger and lighter at the onset of puberty. Heifers fed the high-energy and protein diet were 15 d younger at conception and 14 d younger at calving than heifers fed the conventional diet. Body weight after calving, daily gain during gestation, withers height at calving, body condition score at calving, calving difficulty score, and calf BW were not different. Energy-corrected, age-uncorrected 305-d milk yield was not different, averaging 9,778 kg and 10,069 kg for heifers fed the conventional and intensive diets, respectively. However, removing genetic variation in milk using parent average values as a covariate resulted in a tendency for greater milk from heifers fed the intensive diet. Preweaning costs were higher for heifers fed the intensive diet. However, total costs measured through first lactation were not different. Intensified feeding of calves can be used to decrease age at first calving without negatively affecting milk yield or economics.

The objective of this study was to determine if melatonin fed in the middle of a long day (l6L:8D) reduces mammary parenchymal growth and reduces serum prolactin in prepubertal heifers, thereby mimicking the effects of a short photoperiod. Sixteen prepubertal Holstein heifers were maintained under natural May to August environmental conditions of Michigan plus supplemental lighting to provide a photoperiod of l6L:8D (lights-on 0600-2200 h). At the midpoint of each day, 8 animals were individually fed melatonin (4 mg/100 kg body weight) and 8 were individually fed vehicle (95% ethanol) in 200 g of a grain concentrate mixture. Blood samples were collected at 1-h intervals for 25 h beginning on Day 67. On Day 70 or 72 heifers were slaughtered. No differences were found in body weight gain between melatonin- and vehicle-fed animals. Parenchyma of mammary glands from melatonin-fed heifers had a lower content (24%) and concentration (17%) of deoxyribonucleic acid but a greater concentration of triglyceride (24%) than that of controls. Mean serum prolactin concentration was 27% lower in melatonin-fed animals. In both groups, serum concentrations of prolactin varied throughout the day, with greatest values occurring between 1100 and 1800 h in positive association with changes in ambient temperature. We conclude that melatonin orally administered to prepubertal heifers reduced mammary parenchymal growth and concentration of prolactln in serum. The data support the hypothesis that melatonin mimicks photoperiodic effects on mammary growth and prolactin secretion in cattle.

Beginning at 128 d of pregnancy, Holstein heifers were exposed to 16 h light, 8 h dark (long days; n = 10) or 8 h light, 16 h dark (short days; n = 10) until 35 d before calving when they were killed. Photoperiod had no effect on weight or proportion of extraparenchymal fat or parenchyma in the mammary gland or on amount of fat, DNA, or RNA in mammary parenchyma. Serum prolactin concentration was 1.7-fold greater under long than under short days. Concentration of melatonin in serum was 2.4-fold greater during dark than light periods. Duration of elevated serum melatonin concentration in the dark period was longer in heifers given short days, but magnitude of this increase was lower than that in heifers exposed to long days. In a second experiment, peak amplitude and area of the periparturient surge of serum concentration of prolactin were 1.8-fold and 1.7-fold greater, respectively, in six Holstein heifers exposed to long days than in six heifers exposed to short days. We conclude that photoperiod had no effect on mammary development during pregnancy, but relative to short days, long days increased serum concentration of prolactin during pregnancy, including the period of the periparturient surge of prolactin.

The experimental objective was to determine the effects of feeding prepubertal dairy heifers a high-energy diet for 3, 6, or 12 wk on mammary growth and composition. Holstein heifers (age = 11 wk; body weight = 107 +/- 1 kg) were assigned to 1 of 4 treatments (n = 16/ treatment). The treatment period lasted 12 wk and treatments were H0 (low-energy diet fed for 12 wk, with no weeks on the high-energy diet); H3 (low-energy diet fed for 9 wk, followed by the high-energy diet for 3 wk); H6 (low-energy diet fed for 6 wk, followed by the high-energy diet for 6 wk); and H12 (high-energy diet for all 12 wk). The low- and high-energy diets were formulated to achieve 0.6 and 1.2 kg of average daily gain, respectively. Heifers were slaughtered at 23 wk of age and mammary tissue was collected. A longer duration of feeding the high-energy diet increased total mass of the mammary gland, extraparenchymal fat, and intraparenchymal fat, but did not alter the mass of fat-free parenchymal tissue. When adjusted for carcass weight to reflect differences in physical maturity, the mass of fat-free parenchymal tissue decreased in a linear fashion with a longer duration on the high-energy diet. Total masses of mammary parenchymal DNA and RNA were not different. However, after adjustment for carcass weight, the masses of DNA and RNA decreased as heifers were fed the high-energy diet for a longer duration. The percentages of epithelium, stroma, and lumen, the number of epithelial structures, and the developmental scores of mammary parenchymal tissue were not different among treatments. However, the percentage of proliferating epithelial cells in the terminal ductal units, as indicated by Ki-67 labeling, decreased as heifers were fed the high-energy diet for a longer duration. We concluded that feeding prepubertal heifers a high-energy diet for a longer duration resulted in a linear decrease in both the percentage of mammary epithelial cells that were proliferating and in the mass of fat-free mammary parenchyma per unit of carcass. High-energy feeding hastens puberty and, in this study, decreased mammary epithelial cell proliferation in areas of active ductal expansion. These data are consistent with the idea that feeding heifers a high-energy diet will reduce mammary parenchymal mass at puberty.

The objective was to determine the effects of feeding prepubertal dairy heifers a high-energy diet for a duration of 0, 3, 6, or 12 wk on feed intake, growth, and fat deposition. We also used feed composition, daily intake, and body growth data to evaluate the nutritional model of the 2001 National Research Council (NRC) Nutrient Requirements of Dairy Cattle. Holstein heifers (age = 11 wk; body weight = 107 +/- 1 kg) were assigned to 1 of 4 treatments (n = 16/treatment) designated H0, H3, H6, and H12 and fed a low-energy diet for 12, 9, 6, or 0 wk, followed by a high-energy diet for 0, 3, 6, or 12 wk, respectively. Four heifers were killed initially (11 wk of age) and 64 heifers were killed at the end of the treatment period (23 wk of age). The low-energy diet was formulated to achieve 0.6 kg of average daily gain and contained 16% crude protein, and 45% neutral detergent fiber. The high-energy diet was formulated to achieve an average daily gain of 1.2 kg and contained 18% crude protein and 23% neutral detergent fiber. Actual daily gains averaged over the 12-wk treatment period were 0.64, 0.65, 0.83, and 1.09 kg for the H0, H3, H6, and H12 groups, respectively. Body weight, withers height, hip width, carcass weight, liver weight, and perirenal fat increased in heifers fed a high-energy diet for a longer duration. In addition, percentage of fat increased and percentage of protein decreased in rib sections with a longer duration on the high-energy diet. Uterine and ovarian weights adjusted for body weight decreased when heifers were fed the high-energy diet for a longer duration. The 2001 NRC underestimated dry matter intake of the high-energy diet and overestimated dry matter intake of the low-energy diet. On the basis of actual intakes of each diet, the NRC slightly underestimated gain for the low-energy diet and overestimated gain by 40% for the high-energy diet. The likely explanation for this is that the NRC underestimated the proportion of gain that was fat in the heifers fed the high-energy diet and therefore predicted more body gain per unit of energy intake. We concluded that feeding a high-energy diet for a short duration altered body growth and fat deposition in a time-dependent, linear manner consistent with feeding a high-energy diet for a long duration.

The effects of elevated circulating concentrations of prolactin were examined on neurochemical estimates of activity of dopaminergic neurons in the infundibulum/pituitary stalk of Holstein bull calves (8-10 weeks of age). Activity of these neurons was estimated by measuring the accumulation of dihydroxyphenylalanine, the immediate precursor of dopamine, 15 min after an intravenous injection of the aromatic L-amino acid decarboxylase inhibitor, 3-hydroxybenzylhydrazine. Subcutaneous injections of the dopamine antagonist haloperidol every 6 hr for 1 day increased serum concentrations of prolactin and accumulation of dihydroxyphenylalanine in the infundibulum/stalk. Intravenous infusions of prolactin for 1 or 9 days increased accumulation of dihydroxyphenylalanine in the infundibulum/stalk, indicating that these neurons remain responsive to elevated prolactin for at least 9 days. It is concluded that elevated concentrations of prolactin in blood stimulate dopaminergic neurons in the infundibulum/pituitary stalk of bull calves. We speculate that these neurons may be analogous to the tuberoinfundibular dopaminergic neurons that regulate prolactin in rats.

The objective of this study was to determine if increased energy and protein intake from 2 to 14 wk of age would affect mammary development in heifer calves. At 2 wk of age, Holstein heifer calves were assigned to 1 of 4 treatments in a 2 x 2 factorial arrangement with 2 levels of protein and energy intake (moderate, M; high, H) in period 1 (2 to 8 wk of age) and 2 levels of protein and energy intake (low, L; high, H) in period 2 (8 to 14 wk of age), so that mean initial body weights were approximately equal for all 4 treatments (ML, MH, HL, and HH). The M diet in period 1 consisted of a standard milk replacer (21.3% CP, 21.3% fat) fed at 1.1% of BW on a DM basis and a 16.5% CP grain mix fed at restricted intake to promote 400 g of daily gain, whereas the L diet in period 2 consisted only of the grain mix. The H diet in period 1 consisted of a high-protein milk replacer (30.3% CP, 15.9% fat) fed at 2.0% of body weight on a DM basis and a 21.3% CP grain mix available ad libitum. In period 2, the H diet consisted of just the 21.3% grain mix. Calves were gradually weaned from milk replacer by 7 wk and slaughtered at 8 (n = 11) or 14 wk of age (n = 41). Parenchyma from the distal region, midgland, and proximal region relative to the teat from one half of the udder was collected, fixed, and embedded in paraffin. The other half of the gland was used to determine parenchymal mass, protein, fat, DNA, RNA, and extraparenchymal mass. Total parenchymal tissue, parenchymal DNA, parenchymal RNA, and concentrations of DNA and RNA were higher for calves on the H diet during period 1, but were not affected by diet during period 2. Parenchymal fat percentage was increased by the H diet during period 2. The H diet increased extraparenchymal fat during both periods. The area of parenchyma occupied by epithelium was not affected by treatment, but at the end of period 2, the percentage of proliferating epithelial cells as indicated by Ki67, an marker of cell proliferation, expression was greater for calves on the M diet in period 1 compared with calves on the H diet in period 1. Diets did not influence parenchymal protein percentage or the ratio of RNA to DNA. Higher energy and protein intake from 2 to 8 wk of age increased parenchymal mass and parenchymal DNA and RNA in mammary glands of heifer calves without increasing deposition of parenchymal fat. Diet also influenced histological development of mammary parenchyma and subsequent proliferation of ductal epithelial cells. Implications of these effects for future milk production potential are unknown.

The purpose of this experiment was to determine the role of growth hormone-releasing hormone (GHRH) and somatostatin (SRIH) neurons in mediating α2-adrenergic receptor-induced stimulation of growth hormone (GH) secretion in cattle. Our first objective was to determine if stimulation of α2-adrenergic receptors increases activity of GHRH neurons in the arcuate nucleus (ARC) and/or decreases activity of SRIH neurons in periventricular (PeVN) and ARC nuclei. Clonidine (an α2-adrenergic agonist) or vehicle (saline) were injected i.v. into steers and dual-label immunohistochemistry was performed to quantify the number of GHRH and SRIH neurons expressing Fos and Fos-related antigens (Fos/FRA) as markers of neuronal activity. Clonidine increased concentrations of GH in serum and decreased activity of SRIH neurons in the PeVN, but not in the ARC. Clonidine did not alter activity of GHRH neurons in the ARC. Our second objective was to determine if clonidine decreases secretion of SRIH from perifused slices of hypothalami, which contain perikarya and terminals of GHRH and SRIH neurons, and from explants of hypophysial stalk alone, which contain only terminals of GHRH and SRIH neurons. Clonidine failed to alter release of GHRH or SRIH from hypothalamic slices, but stimulated release of GHRH from explants of hypophysial stalk. Blockade of SRIH receptors enabled clonidine to stimulate release of GHRH from slices of hypothalami, but also stimulated release of SRIH. These results suggest that α2-adrenergic-induced secretion of GH occurs via a dual mechanism involving inhibition of SRIH neurons in the PeVN and direct stimulation of GHRH release from axon terminals in the median eminence.

To determine effects of rapid prepubertal growth on first-lactation milk production, Holstein heifers were randomly assigned to one of three treatments. Thirty-five heifers were fed a standard diet to meet NRC recommendations and produce 0.8kg of body weight (BW) gain/d (standard). Thirty-five heifers were fed a diet with higher energy (2.8 Mcal of metabolizable energy/kg) and protein (19.7% crude protein; high diet) to produce 1.2kg of BW gain/d (high). Thirty-five heifers were fed the high diet and injected daily with bovine somatotropin (bST) (25µg/kg of BW; high-bST). Diets were fed and bST was injected from 135kg of BW until pregnancy was confirmed. Heifers were inseminated after BW exceeded 363kg. Pregnant heifers were commingled and fed similar diets through gestation, parturition, and lactation. High and high-bST heifers had greater prebreeding average BW gains than standard heifers. Conversely, standard heifers had a greater average BW gain during gestation than high and high-bST heifers. High and high-bST heifers were approximately 90 d younger than standard heifers at first insemination and first parturition. Postpartum BW, body condition scores, and withers heights at parturition, and calving ease scores were not different among treatments. Standard heifers produced 14% more milk than high heifers but not more than high-bST heifers. The high-protein, high-energy diet decreased age at first parturition and first-lactation milk production, but did not affect reproduction. Injection of bST during the pre-pubertal growth period combined with the high diet decreased age at first parturition without reducing milk production.

Secretion of growth hormone (GH) is reduced for several hours after feeding when access to feed is restricted to a 2-hr period each day. We hypothesized that increased secretion of insulin after feeding inhibits release of GH from the anterior pituitary gland. Our objectives were to determine whether: 1) alloxan prevents concentrations of insulin from increasing after feeding steers; 2) concentrations of GH remain high after feeding alloxan-treated steers; and 3) GH-releasing hormone (GHRH) stimulates greater release of GH in alloxan-treated, than in control, steers after feeding. Steers were injected iv with either saline (control) or with alloxan (110 mg/kg) (n = 4 per group). Concentrations of insulin were not different (P = 0.61) between control and alloxan-treated steers before feeding (87.5 ± 33.6 pmol/l). However, alloxan prevented insulin from increasing (P < 0.001) after feeding (131.8 pmol/l) compared with control steers (442.0 pmol/l) (pooled SEM = 47.5). Overall, GH was higher (P < 0.05) in alloxan-treated (6.4 ng/ml) than in control steers (3.7 ng/ml) (pooled SEM = 0.7), but GH decreased (P < 0.001) after feeding in both groups. Iv injection of GHRH stimulated release of GH 1 hr before, but not when injected 1 hr after feeding (P < 0.001). In addition, net areas under the GH curve were not significantly different between control and alloxan-treated groups. We conclude that increased concentrations of insulin after feeding do not mediate feeding-induced suppression of GH secretion in steers.

Forty Holstein heifers [body weight (BW) = 126 kg] were blocked by BW into groups of 4, and, within each block, heifers were randomly assigned to one of four treatments. Twenty heifers had ad libitum access to a diet formulated to produce a BW gain of 0.8 kg/d (control diet), and 20 heifers had ad libitum access to a diet formulated to produce a BW gain of 1.2 kg/d. (high diet). Half of the heifers fed each diet were injected daily with bovine somatotropin (bST; 25 micrograms/ kg of BW). The high diet increased daily BW gain as well as body condition score. Injection of bST also increased daily BW gain, but did not affect body condition score. The high diet reduced age at puberty by 58 d, but did not affect BW, withers height at puberty, or pelvic area at slaughter. Injection of bST had no effect on age at puberty, but increased BW, withers height at puberty, and pelvic area at slaughter. The high diet did not affect mammary parenchymal DNA, RNA, or the ratio of RNA to DNA. The injection of bST increased mammary parenchymal DNA, RNA, and the ratio of RNA to DNA. The high diet was more cost effective for rearing dairy heifers from 120 d of age to potential breeding size (> or = 363 kg of BW and postpubertal) than was the control diet. In conclusion, the high protein, high energy diet increased growth rate without detrimental effects on mammary development. Injection of bST increased BW, skeletal size, and mammary development.

Holstein cows received 12mg/d of growth hormone-releasing factor (continuous i.v. infusion, n=5), 14mg/d of bST (single daily i.m. injection, n=8), or no treatment (controls, n=8) for 60 d. Compared with controls (31.6kg/d), bST and growth hormone-releasing factor increased milk yield to 34.2 and 37.0kg/d, respectively. The increase in milk yield induced by the growth hormone-releasing factor was greater than that for bST. Milk yield was not different among groups following cessation of treatment. Milk energy output was 24.2Mcal/d in controls, and growth hormone-releasing factor increased milk energy output to 28.5Mcal/d. Milk energy output of cows receiving bST was 26.1Mcal/d. Growth hormone-releasing factor increased DMI (23.2kg/d) over that of controls (21.1kg/d), whereas bST (21.5kg/d) did not. Relative to controls, bST increased averaged daily serum somatotropin from 1.3 to 7.6ng/ml and insulin-like growth factor-I from 67.5 to 116.0ng/ml. Relative to bST, growth hormone-releasing factor increased serum somatotropin to 16.3ng/ml and insulin-like growth factor-I to 202.6ng/ml. Relative to control (115.8meq/dl) and bST (158.1meq/dl), growth hormone-releasing factor increased plasma NEFA (230.3meq/dl). During treatment, calculated energy balance was negative for cows receiving growth hormone-releasing factor but positive for bST and control cows. Milk composition, body condition score, BW, and apparent digestibility of DM were not different among treatments. We conclude that i.v. infusion of 12mg/d mg of growth hormone-releasing factor has greater galactopoietic activity than i.m. injections of 14mg/d of bST. These data support the concept that the galactopoietic effects of growth hormone-releasing factor are mediated via increased secretion of somatotropin and insulin-like growth factor-I.

The effects of ambient temperature on serum concentrations of prolactin and neurochemical estimates of activity of dopaminergic neurons projecting to the infundibulum/pituitary stalk were investigated in Holstein bull calves. Accumulation of 3,4-dihydroxyphenylalanine (DOPA) in the infundibulum/pituitary stalk after intravenous injection of a decarboxylase inhibitor was used to estimate activity of these dopaminergic neurons. Increasing ambient temperature from 21 to 33 degrees C for 22 hr increased serum concentrations of prolactin and decreased activity of the dopaminergic neurons. Conversely, reducing ambient temperature from 22 degrees C to 11 degrees C decreased serum concentrations of prolactin and increased activity of these dopaminergic neurons. It is suggested that alterations in activity of dopaminergic neurons terminating in the infundibulum/pituitary stalk of bull calves may mediate acute temperature-induced changes in secretion of prolactin.

Twenty-four Holstein cows were infused intravenously with sterile water (placebo) or 1, 3, or 12 mg of recombinant bovine somatotropin-releasing factor 1-45-homoserine lactone/d for 60 d. Relative to placebo (22.8 kg/d), 3 and 12 mg of somatotropin-releasing factor increased yield of milk to 28.8 and 33.3 kg/d during infusion. At 1 mg of somatotropin-releasing factor, milk averaged 27.5 kg/d during infusion but was increased above placebo only through 39 d. After infusion of 12 mg somatotropin-releasing factor ended, milk (26.4 kg/d) remained above placebo amounts (20.6 kg/d) for 15 d. Three and 12 mg of somatotropin-releasing factor increased serum somatotropin from .7 (placebo) to 8.2 and 10.3 mg/ml when averaged across 1, 30, and 59 d, whereas 1 mg increased somatotropin to 5.8 ng/ml after 1 d but had no effect at 30 or 59 d. Within 17 h of cessation of somatotropin-releasing factor infusion, serum concentrations of somatotropin were similar across all groups. On d 59, 3 and 12 mg infusions increased insulin-like growth factor I from 115.8 (placebo) to 204.7 and 261.4 ng/ml of serum. We conclude that somatotropin-releasing factor increased serum concentrations of somatotropin and milk yield in a dose-dependent manner for at least 60 d. Also, galactopoietic effects of somatotropin-releasing factor persisted for 15 d independent of increased concentrations of somatotropin in serum following withdrawal of somatotropin-releasing factor.

The objectives were to determine if photoperiods of 8 h light:16 h dark (8L:16D) and 16L:8D affect time of day when preovulatory surges of luteinizing hormone (LH) and follicle stimulating hormone (FSH) occur and if photoperiods affect diestrus and estrous concentrations of LH, FSH and prolactin (PRL). Postpubertal Holstein heifers were assigned to receive either 8L:16D (n - 9) or 16L:8D (n = 9) from September 21 through January 31. Hormone concentrations were determined in serum collected at 2-h intervals during diestrus and estrus of a single estrous cycle in autumn and again 4 mo later, during a single estrous cycle in winter. Neither photoperiod nor season affected time of day at which preovulatory LH and FSH surges occurred in heifers. The LH surges did not differ in amplitude and duration within and between photoperiods and within individual animals. In 29 of 33 surges, peak concentrations of FSH coincided with peaks of LH. Peak concentrations of FSH were greater during the winter than during autumn in heifers exposed to 8L:16D, but were not different between autumn and winter in heifers exposed to 16L:8D. Between autumn and winter, surges of FSH were similar in magnitude and duration within individual animals. In comparison with 8L:16D, PRL was increased in heifers that received 16L:8D in autumn, but photoperiod had no effect on PRL during winter. Concentrations of PRL were increased at estrus relative to diestrus in autumn and winter. It is concluded that photoperiods of 8 and 16 h do not affect the timing, amplitude or pattern of preovulatory surges of LH or FSH, the rise in PRL associated with estrus, or length of estrous cycles in postpubertal Holstein heifers.

Milk production and dry matter intake of 21 cows subjected to 16 h of fluorescent light and 8 h dark and of 21 cows subjected to natural light 9 to 12 h daily between October 25 and March 14 were measured beginning in early (37 to 74 days postpartum) and late (94 to 204 days postpartum) lactation. Cows that received 16 h of fluorescent light produced 6.7% (1.4 kg) more milk per day (adjusted for parity and pretreatment production) than cows exposed to natural photoperiods. Increases of milk production with 16 h of fluorescent light were similar for early and late lactation. Photoperiod did not alter percent of fat in milk. Dry matter intake increased 6.1% for cows in 16 h of light, and this increase could account for increased milk yields. Basal prolactin in serum and that released by thyrotropin releasing hormone were 1.5 to 1.8 times greater for cows exposed to 16 h of light than for cows in 9 to 12 h of natural light daily. Photoperiod did not affect release of prolactin by milking. Cold ambient temperatures reduced basal prolactin and prolactin released by thyrotropin releasing hormone but had no effect on concentrations of growth hormone or glucocorticoids. Compared with cows in late lactation, cows in early lactation released 2.4 times more prolactin after milking, but they released similar amounts of prolactin after thyrotropin releasing hormone. Photoperiod did not affect concentrations of growth hormone or glucocorticoids in blood sera.

Effects of 16 (16 light:8 dark) and 8 (8L:16D) h of daily light were compared with continuous light (24L:0D) exposure on prolactin (PRL) concentrations in serum of prepubertal bulls. Concentrations of PRL in serum were 2 to 3 fold greater in bulls exposed to 24L:0D or 16L:8D as compared with 8L:16D. However, PRL concentrations attained a maximum approximately 3 weeks later in calves exposed to 24L:0D than in calves given 16L:8D. Continuous low intensity (11 to 16 lux) lighting supplemented with 16 or 8 h of high intensity (449 to 618 lux) light per day increased PRL concentrations in serum of prepubertal bulls 1.5 to 2.5 fold relative to 8L:16D (470 lux). We found that relative to 8L:16D, 1) photoperiods of 16 or 24 h of light per day increased serum concentrations of PRL in prepubertal bulls; however, the time required to achieve maximum PRL concentrations was longer in animals exposed to 24L:0D, 2) continuous low intensity lighting supplemented with 16 or 8 h of high intensity daily light also increased concentrations of PRL in serum.

Effects of photoperiod on growth, carcass composition and serum concentrations of prolactin, growth hormone and cortisol were determined in prepubertal and postpubertal Holstein heifers. Forty-two prepubertal (avg body wt 84 +/- 3.0 kg) and 42 postpubertal (avg body wt 303 +/- 7.1 kg) Holstein heifers were utilized. Ten prepubertal and 10 postpubertal heifers were slaughtered before treatment began to obtain initial carcass data. The remaining 32 prepubertal and 32 postpubertal heifers were paired by body weight and randomly assigned to short-day (8 h of light: 16 h of dark) or long-day (16 h of light: 8 h of dark) photoperiods. After exposure to treatments for an average of 139 d, 10 prepubertal and 10 postpubertal heifers from each photoperiod treatment were slaughtered. In prepubertal heifers, photoperiod did not affect (P greater than .10) average daily body weight gain, carcass weight, carcass composition, accretion of carcass fat and carcass protein, or serum concentrations of prolactin, growth hormone or cortisol. However, prepubertal heifers exposed to long-day photoperiods had reduced (P less than .01) urinary N tau-methylhistidine excretion compared with heifers given short-day photoperiods. Postpubertal heifers exposed to short-day photoperiods had greater average body weight daily gain than animals exposed to long-day photoperiods. Although there was no effect of photoperiod (P greater than .10) on carcass or fat depot weights, postpubertal heifers exposed to short days had greater (P = .06) percentages of fat and reduced (P = .07) percentages of protein in the soft tissue of the 9-10-11 rib sections. Fat accretion was greater (P less than .05) in carcasses of postpubertal heifers exposed to short days than heifers given long-day photoperiods, but there was no effect (P greater than .10) of photoperiod on protein accretion. Photoperiod did not affect serum concentrations of growth hormone and cortisol, but serum prolactin tended (P less than .10) to be greater in postpubertal heifers exposed to long days. Under the conditions of this experiment, we conclude that exposure to short-day photoperiods stimulated body weight gain and fat accretion in postpubertal but not prepubertal Holstein heifers.

To determine effects of photoperiod and ovaries and their interactions on live-weight (LW) gain, carcass composition, growth hormone (GH), insulin (INS) and prolactin (PRL), crossbred beef heifers were utilized. Heifers (no. = 70) were blocked by LW and assigned to a pre-treatment slaughter group for estimation of initial carcass composition or to treatments in a 2 × 2 factorial experiment (no. = 14 per treatment). Main effects were: photoperiod (8 h light (L): 16 h dark (D) v. 16L: 8D) and ovaries (intact (INT) v. ovariectomized (OVX)). Heifers were given a maize-based mixed diet (115 g protein and 11·5 MJ metabolizable energy per kg dry matter) ad libitum once per day at 07.30 h. On days 64 and 138, blood samples were taken every 30 min for 10 h from five heifers in each treatment. On day 144 treated heifers were slaughtered. Relative to OVX heifers, INT heifers had greater (P < 0·01) average LW gain (1·03 v. 1·17 kg/day), carcass weight (252 v. 270 kg) and carcass protein accretion rates (68 v. 82 g/day) but carcass fat accretion was not affected (P < 0·l; 381 v. 399 g/day). Compared with 8L: 16D, exposure to 16L: 8D non-significantly increased LW gain more in OVX heifers (16 kg) than in INT heifers (3 kg). Photoperiod did not significantly influence weight or composition of the carcass. There was no significant interaction between photoperiod and ovaries on carcass composition. Across all heifers GH declined (P < 0·05) and INS and PRL increased (P < 0·05) from day 64 to 138. Compared with 8L: 16D, exposure to 16L: 8D increased PRL on day 64 (P < 0·05; 13·4 v. 28·5 u.g/1) and decreased INS averaged across days 64 and 138 (P = 0·l; 0·71 v. 0·55 u/l) but had no effect on GH. GH, INS and PRL did not differ between INT and OVX heifers. It is concluded that ovariectomy of heifers reduces LW gains, carcass weights and accretion of protein, and that exposure to 16L: 8D partially prevents the loss in LW gain.

The objective was to determine whether dairy cows fed supplemental iodine daily at 2.5 or 5.0 mg per kg body weight for 49 wk had altered thyroid status relative to controls fed no supplemental iodine. Average daily dose of iodine was 1.6 and 3.3 g. Iodine as ethylene diamine dihydriodide was fed to Holstein cows beginning at 8 to 10 wk of lactation, for the remainder of that lactation, through the dry period, and into the next lactation. On day 341 after onset of iodine feeding, each cow was injected intravenously with 15 microgram thyrotropin releasing hormone per 100 kg body weight. Thyrotropin in jugular blood collected before injection of releasing hormone averaged 7.6, 6.1, and 8.2 ng/ml for cows given 0, 2.5, and 5.0 mg iodine/kg body weight; there were no differences between means. Releasing hormone increased thyrotropin, thyroxine, and tri-iodothyronine in serum of all cows, but increases were not affected by quantity of dietary iodine.

Two experiments were conducted to determine if feeding melatonin alters plasma concentrations of melatonin, growth and carcass composition of postpubertal beef heifers exposed to 16 h light (L):8 h dark (D). In Exp. 1, 16 heifers were blocked by initial body weight (318 +/- 5.6 kg). Four heifers were killed before starting the melatonin treatment to obtain initial carcass composition. Six heifers received vehicle (95% ethanol) and six were fed melatonin (4 mg/100 kg body weight) daily for 58 d at 1330 to coincide with the middle of the 16-h light period. On d 59 heifers were slaughtered. Melatonin feeding increased the percentage of fat in rib (P less than .05) and longissimus muscle (LD; P less than .10) and carcass fat accretion 28% (P less than .09) but reduced the percentage of protein 8% in rib (P less than .05) and carcass protein accretion 30% (P less than .09). Other measures in the carcass and body weight gain were not affected (P greater than .10) by feeding melatonin. Plasma concentrations of melatonin increased (P less than .01) from 10 to 140 pg/ml within 30 min of feeding melatonin. In Exp. 2, 24 heifers were blocked by initial body weight (348 +/- 13.7 kg). Eight heifers were killed initially, eight received vehicle and eight were fed melatonin for 63 d as described in Exp. 1. Melatonin did not influence (P greater than .10) body weight gain or any measure in the carcass; however, these heifers were fatter (40.1%) than those in Exp. 1 (30.9%) at the beginning of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

After 8 wk exposure to 8 h of light per day, prolactin (PRL) averaged 18.3 ng/ml of serum in eight male calves. Four calves then received 16 h of light per day; 6 wk later (age 14 wk) PRL averaged 93.8 ng/ml of serum, whereas PRL averaged 36.9 ng/ml of serum in four calves maintained under 8 h of daily light. By wk 20, PRL was not different in calves exposed to 16 or 8 h of daily light, averaging 34.7 and 17.2 ng/ml serum. Testosterone averaged .43 ng/ml of serum at wk 8 but was greater at wk 14 in calves receiving 16 h of light daily when compared with controls receiving 8 h of light (1.92 vs. .97 ng/ml of serum). Testosterone concentrations were not different between photoperiod treatments at wk 20. Luteinizing hormone (LH) concentrations were unaffected by photoperiod. In a second experiment, four male calves were castrated at approximately 2 wk of age while four similar controls were left gonadally intact. After 8 wk exposure to 8 h of light per day, PRL averaged 12.3 ng/ml of serum in all calves. After 6 wk exposure to 16 h of light per day, PRL in serum increased in castrates to 48.0 ng/ml and in controls to 59.8 ng/ml. We conclude that serum concentrations of PRL and testosterone, but not LH, increased in bull calves receiving 16 h of light daily relative to calves receiving 8 h of light, and that the PRL response to photoperiod is independent of the testes. However, 16 h light-induced stimulation of serum concentrations of prolactin is not maintained indefinitely.

In a first experiment growth hormone was determined in serum of lactating cows infused intravenously with bovine growth hormone-releasing factor for 24 h. Concentrations of growth hormone increased 5 times above placebo after 3.125, 6.25, 12.5, 25.0, or 50.0 mg releasing factor/cow per 24 h. Releasing factor increased the pulsatile nature of growth hormone release. In a second experiment we determined effects of intravenous infusions of releasing factor for 20 d on growth hormone and lactation in primiparous cows (n = 5/treatment; 144 +/- 7 d after parturition). Milk yield of placebo-infused cows averaged 26.5 +/- 1.7 kg/d during d 6 to 20 of infusion. Infusions of 1 and 3 mg releasing factor/cow per 24 h increased milk yield 11 and 23%, respectively. Releasing factor had only small effects on milk composition, net energy intake, and BW. Releasing factor did not affect energy efficiency of milk production (energy output in milk per unit of net energy intake) when corrected for BW changes. Average growth hormone across d 1, 10, and 19 of infusion was 2.1, 4.1, and 6.8 ng/ml serum for placebo, 1, and 3 mg releasing factor, respectively. Infusions of bovine growth hormone-releasing factor: 1) increased mean and pulsatile release of growth hormone during 24 h and 20 d, 2) increased milk yield in a dose-dependent manner, and 3) did not affect BW-corrected energy efficiency of milk production.

Our objective was to determine the relationship between energy balance and secretion of progesterone in lactating dairy cows. Eight primiparous and 24 multiparous lactating Holstein cows were studied from parturition to 100 d postpartum or conception. Cows calved normally and remained healthy throughout the study. All cows were fed ad libitum a total mixed diet formulated to satisfy requirements for maintenance and lactation. Intake of feed and production of milk per cow were measured twice daily. Body weight was determined weekly. Daily energy balance was determined by subtracting energy required for maintenance and lactation from intake of energy. Concentrations of progesterone were determined in milk sampled every 3rd d. For at least 4 successive d postpartum, 81% of cows were in negative energy balance. Variation in energy balance was explained largely by intake of energy. Duration of luteal phases was not associated with energy balance. Energy balance within 9 d postpartum was correlated positively with concentration of progesterone within second and third postpartum luteal phase. Postpartum interval to nadir and magnitude of nadir of energy balance interacted to reduce progesterone within second and third postpartum estrous cycles. Thus, in lactating cows, secretion of progesterone is reduced by spontaneous caloric deficit and is modulated by timing and magnitude of maximal caloric deficit. Spontaneous caloric deficit is a potential source of infertility in lactating dairy cows.

In each of two experiments, 70 crossbred steers were blocked by BW and assigned to initial slaughter groups or to treatments in a 2 x 2 design. In Exp. 1, treatments were 168 d of photoperiod (8 h of light [L]:16 h of dark [D] or 16L:8D) and plane of nutrition (high energy [HPN] or low energy [LPN]). On d -22, 67 and 155, blood was sampled every 20 min for 8 h. Relative to LPN, HPN increased (P less than .01) ADG by 28%, carcass weight by 26% and accretion of carcass fat by 109% and carcass protein by 20%. On d 155, compared with LPN, HPN increased (P less than .01) serum insulin (INS; 1.09 vs .64 ng/ml) and lowered (P less than .05) growth hormone (GH; 2.14 vs 3.70 ng/ml), but prolactin was not affected. Photoperiod did not affect BW gains, carcass composition or serum hormones. In Exp. 2, treatments were 113 d of photoperiod (8L:16D or 16L:8D) and Synovex-S implant (presence [IMP] or absence [NONIMP]). On d 93, blood was sampled every 30 min for 10 h. Relative to NONIMP, IMP increased (P less than .01) ADG by 12% and accretion of carcass protein by 16%. Implants did not affect carcass weight or accretion of fat. Compared with NONIMP, IMP increased (P less than .05) GH (3.16 vs 2.39 ng/ml) and INS (.68 vs .46 ng/ml) but did not affect PRL. Photoperiod did not affect BW gain, carcass composition or serum hormones. We conclude that photoperiod fails to influence growth and carcass composition of steers.

Body growth and dry matter intake were measured in three groups of 16 Holstein heifers exposed to (1) natural, (2) 16 hr light: 8 hr dark (16L:8D) or (3) 24L:0D photoperiods for November 11 to March 10. Average daily gain (ADG) of heifers subjected to 16L:8D was 11 (P less than .05) and 17% (P less than .02) greater than ADG of animals receiving 24L:0D or natural photoperiod, respectively. Heifers subjected to 16L:8D consumed 6.9 and 8.3% more (P less than .01) dry matter per day than did animals exposed to 24L:0D or natural photoperiod, respectively. Yet feed to gain ratio of heifers exposed to 16L:8D was lower than that of heifers exposed to 24L:0D or natural photoperiod. Serum prolactin (PRL) and growth hormone (GH) were measured in six heifers in each treatment group at 30-min intervals, and serum total glucocorticoids were measured at 2-hr intervals over a 6-hr period on December 26, February 6 and March 7. Concentrations of serum PRl remained low (less than 3 ng/ml) regardless of photoperiod treatment; this would be expected, however, because mean ambient temperatures were below 0 C on all sampling days. Serum GH and total glucocorticoids were likewise unaffected by photoperiod treatment. This study demonstrates that an 8-hr period of darkness is necessary to achieve increases in weight gain when Holstein heifers are supplemented with light during the autumn-winter season in Michigan, but the mechanisms whereby photoperiod affects body growth remain unknown.

Serum growth hormone was determined in lactating cows following repeated intravenous injections of growth hormone-releasing factor. A given dose was injected every 4 h for 24 h in a 4 (cow) X 4 (d) Latin square. Growth hormone increased similarly above controls after 10, 20, or 40 micrograms releasing factor/100 kg body weight. In another experiment the effects on lactational performance and growth hormone responses of cows to repeated injections of releasing factor for 10 d were determined in a 2 (cow) X 2 (period) Latin square crossover. Administration of 20 micrograms releasing factor/100 kg body weight to 16 Holstein cows (lactating 4.5 to 7.5 mo) every 4-h for 10 d increased milk yield from 25.4 to 27.7 kg/d and increased total fat, protein, and lactose 11% above controls. Releasing factor did not affect milk composition or feed intake. Peak growth hormone response to releasing factor was similar between d 1 (19.9 ng/ml) and 10 (24.4 ng/ml). Exogenous growth hormone-releasing factor administered to lactating Holstein cows at the doses tested: 1) increases growth hormone consistently, although the response is not dose dependent, 2) is galactopoietic, 3) causes an apparent increase in feed to milk conversion, and 4) increases growth hormone to at least the same magnitude on d 10 as on d 1.

Concentrations of prolactin in serum increased 1.8- to 7.8-fold within 6 weeks after duration of daily light was shifted from 8 to 16 hr. In comparison with cool-white fluorescent light, this increment in concentration of prolactin was similar when a light source that simulates natural sunlight (Vita-Lite), or incandescent, high-pressure sodium, or mercury vapor lamps were used. Regardless of light source, increasing the duration of daily light from 8 to 16 hr during warmer months (Aug) resulted in a greater magnitude of increase in mean prolactin concentrations as compared with increases observed during cooler months (Feb). We conclude that in prepubertal bulls, secretion of prolactin increases similarly when duration of light from lamps with different spectral properties is increased from 8 to 16 hr daily.

Three experiments were conducted to determine serum growth hormone (GH) response of bull calves (N = 4; 83 kg body wt) to iv injections and infusions of human pancreatic GH-releasing factor 1-40-OH (hpGRF). Peak GH responses to 0, 2.5, 10, and 40 micrograms hpGRF/100 kg body wt were 7 +/- 3, 8 +/- 3, 18 +/- 7, and 107 +/- 55 (mean peak height +/- SEM) ng/ml serum, respectively. Only the response to the 40-microgram dose was greater (P less than 0.05) than the 0-microgram dose. Concentrations of prolactin in serum were not affected by hpGRF treatment. In calves injected with hpGRF (20 micrograms/100 kg body wt) at 6-hr intervals for 48 hr, GH increased from a mean preinjection value of 3.1 ng/ml serum to a mean peak response value of 70 ng/ml serum. Differences in peak GH response between times of injection existed within individual calves (e.g., 10.5 ng/ml vs 184.5 ng/ml serum). Concentrations of GH in calves infused continuously with either 0 or 200 micrograms hpGRF/hr for 6 hr averaged 7.4 +/- 3 and 36.5 +/- 11 ng/ml serum, respectively (P less than 0.05). Concentrations of GH oscillated markedly in hpGRF-infused calves, but oscillations were asynchronous among calves. We conclude that GH response of bull calves to hpGRF is dose dependent and that repeated injections or continuous infusions of hpGRF elicit GH release, although magnitude of response varies considerably. We hypothesize that differences in GH response to hpGRF within and among calves, and pulsatile secretion in the face of hpGRF infusion may be related to the degree of synchrony among exogenous hpGRF and endogenous GRF and somatostatin.

Concentration of serum growth hormone was increased and feed intake was reduced in lactating dairy cows fed an 84% concentrate diet supplemented with either 100.8 g MgO or 121.2 g of Mg(OH)2. Analysis of serum growth hormone, feed intake, and serum Mg showed an interaction of serum Mg and feed intake, which suggests low concentrations of serum Mg lessen the increase of concentration of serum growth hormone caused by reduced feed intake. Also, compared with control, treatments with Mg supplementation and reduced feed intake increased growth hormone concentration 12 d into the subsequent treatment.

Early temporal changes in concentrations of prolactin (PRL) in serum after a sudden change in photoperiod and daily responsiveness to PRL-releasing and inhibiting factors were investigated in prepubertal Holstein bull calves exposed to different photoperiods. In calves switched from 8-hr light: 16-hr dark to 16-hr light:8-hr dark, there was no observable change in the daily pattern of serum concentrations of PRL after 1, 2, or 4 days. On the other hand, in animals switched from 16-hr light:8-hr dark to 8-hr light:16-hr dark, there was a consistent increase in serum PRL from 33.4 ng/ml on Day 0 to maximum values of 57.3, 62.7, and 78.9 ng/ml between 14 and 18 hr after onset of light on Days 1, 2, and 4, respectively. Thus, absence of light allowed expression of a daily rhythm in serum concentrations of PRL that persisted for at least 4 days after the photoperiod switch. There were no differences in L-dopa inhibition of PRL release in animals exposed to 16-hr light:8-hr dark at 3 or 15 hr after onset of light. However, thyrotropin-releasing hormone-induced release of PRL was greater 3 hr after onset of light (11 hr after onset of dark) compared with release at 9, 15, and 21 hr after onset of light in animals exposed to 16-hr light:8-hr dark, but not in bulls exposed to 8-hr light:16-hr dark. The results provide evidence that the cue for the putative photosensitive period of PRL secretion in cattle may be more closely associated with onset of dark, not onset of light.

Changing daily exposure of prepubertal bulls from 8 hr of light: 16 hr of dark (8L: 16D) to 16L:8D or 6L:8D:2L:8D increased basal secretion of prolactin 418% 6 weeks later. When daily exposure was changed from 8L:16D (6 weeks) to 6L:14D:2L:2D (6 weeks), basal secretion of prolactin increased only 173%. Among photoperiod exposures, prolactin released into blood after injection of 33 μg/100 kg body weight of thyrotropin-releasing hormone paralleled the changes described for basal conditions. There was no repeatable diurnal secretory pattern for secretion of prolactin. The data support the hypothesis that cattle possess a photosensitive rhythm for secretion of prolactin.

Effects of photoperiod and plane of nutrition on growth, serum concentrations of prolactin (PRL) and growth hormone (GH) and puberty were assessed in Holstein heifers. Sixty pre-pubertal heifers were assigned to one of four treatment groups arranged in a 2 X 2 factorial. The two main effects were photoperiods of 8 h light: 16 h dark (8L:16D) vs 16L:8D, and a low vs high plane of nutrition. Heifers on the low plane of nutrition were fed a diet formulated to achieve a body growth rate of approximately .7 kg/d. Daily feed intake was restricted and similar in both groups of low plane heifers subjected to either 8 or 16 h of light daily. Heifers on the high plane of nutrition were fed ad libitum to achieve a growth rate greater than 1 kg/d. Body weight was recorded every month for 5 mo. The PRL and GH concentrations were measured at d 9, 53 and 132 in serum collected every 30 min for 6 h from five heifers in each treatment group. Progesterone was monitored biweekly in all heifers as an index of puberty (greater than 1 ng/ml). Heifers subjected to 8L:16D-low plane, 16L: 8D-low plane, 8L:16D-high plane or 16L:8D-high plane gained .61, .72, .98 and 1.08 kg/d, respectively. In the same treatment order, averaging across all bleedings, concentrations of PRL were 32, 37, 38 and 46 ng/ml serum, and GH averaged 10.9, 9.3, 9.8 and 9.0 ng/ml serum. Similarly, body weight at puberty averaged 268, 257, 278 and 268 kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty prepubertal heifers (averaging 155 kg body weight) were assigned to one of four treatment groups in an experiment of 2 X 2 factorial design. The main effects were photoperiods of 8 h light:16 h dark (8L:16D) vs 16L:8D, and LOW vs HIGH plane of nutrition. Heifers on the LOW plane of nutrition were fed to achieve a growth rate of approximately .7 kg/d; daily feed intake was restricted with no orts and was identical in both groups of heifers subjected to either 8 or 16 h of light daily. Heifers on the HIGH plane of nutrition were fed ad libitum to achieve a growth rate greater than 1 kg/d. All heifers were slaughtered during the luteal phase of an estrous cycle at an average body weight of 337, 334, 360 and 349 kg for 8L:16D-LOW plane, 16L:8D-LOW plane, 8L:16D-HIGH plane and 16L:8D-HIGH plane groups, respectively. Average time on treatment was 233, 236, 206 and 181 d and average estimated carcass weight gain was .39, .40, .55 and .61 kg/d, respectively. Within LOW or HIGH planes of nutrition, photoperiod did not affect live body weight gains. A photoperiod of 16L:8D, compared with 8L:16D, increased protein content in the 9-10-11th rib section of heifers on HIGH nutrition (16.2 vs 14.6%), but not in heifers fed the LOW plane of nutrition (15.5 vs 16.1%). However, within 8L:16D groups, HIGH plane reduced rib section protein content as compared with LOW plane of nutrition (14.6 vs 16.1%); there was no difference observed within 16L:8D groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Pineal tissue was removed from eight 6-wk-old bull calves (PX), whereas eight similar calves received sham pinealectomies (SPX). Before and after surgery, calves received 8 h of light (L):16 h of darkness (D) daily until 20 wk of age (wk 0 of experiment), at which time eight calves (four PX and four SPX) were maintained under 8L:16D for 12 additional wk, whereas the remaining eight calves received 16L:8D. At 0, 4, 8 and 12 wk of experiment, blood was collected from each animal for 26 h at 30-min intervals. Melatonin in SPX calves at wk 12 increased from 16.2 pg/ml of plasma when lights were on to 81.6 pg/ml during lights off, whereas in PX calves the nocturnal increase was absent. However, the nocturnal surge did occur in three PX calves on 8L:16D treatment, and those animals were excluded from calculations and analysis. At wk 0, prolactin (PRL) averaged 47 ng/ml among all calves. By wk 4 PRL increased (P less than .01) to 80 and 96 ng/ml in PX and SPX calves receiving 16L:8D, respectively; PRL averaged 53 and 48 ng/ml, respectively in PX and SPX calves maintained on 8L:16D. Prolactin was greater (P less than .05) through wk 12 in PX (64 ng/ml) and SPX (64 ng/ml) calves receiving 16L:8D than in calves exposed to 8L:16D, which remained unchanged (54 and 48 ng/ml). Testosterone was unaffected by photoperiod, but tended to be less (P = .13) in plasma of PX than of SPX calves at wk 0 (.90 vs 1.45 ng/ml of plasma).(ABSTRACT TRUNCATED AT 250 WORDS)

In two experiments, 17-wk-old Holstein bulls exposed to 16 (Exp. 1) or 24 h (Exp. 2) of light daily were compared with bulls given 8 h of light. Blood was sampled at 30-min or 120-min intervals for 48 h at the beginning and again after 4 wk of light treatment. Melatonin concentrations varied episodically in serum, and means were 1.6-fold to 5.1-fold greater during darkness than during light periods. Continuous lighting abolished the nocturnal increase in concentrations of melatonin in three of four calves. Prolactin (PRL) was greater (P less than .05) in calves receiving 16 h (30.9 ng/ml of serum) than in calves receiving 8 h (7.0 ng/ml) of light daily. Prolactin was not different between calves receiving 24 or 8 h of light daily. In a third experiment, one pinealectomized (PX) and two sham PX (SPX) calves were exposed to continuous lighting and infused with melatonin for 16 h/d for 5 wk, and one PX and two SPX calves were infused for 8 h daily. Melatonin infusion increased average concentrations of melatonin in serum 7.2-fold to 18-fold above baseline concentrations. Duration of melatonin infusion did not affect PRL (21.0 vs 20.8 ng/ml of serum). Also, surgical treatment did not affect PRL concentrations. Similarly, in a fourth experiment, PRL in postpubertal heifers fed melatonin to mimic and 8L:16D photoperiod averaged 27.1 ng/ml of serum, which was not different from PRL in heifers receiving 16L:8D and fed vehicle (32.6 ng/ml). We conclude that PRL and melatonin are each affected by photoperiod but are not casually related in cattle.