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ABSTRACT. The present study was designed to determine the effects of physiological stress on milk-somatic cell counts (SCC) and function of bovine peripheral blood leukocytes (PBL). Nine healthy lactating cows were used in the examination. Five cows were transported 100 km for 4 hr (transported group; TG), and 4 cows were penned (non-transported group; NTG). Blood and milk samples were collected at 0, 2, and 4 hr after loading, and at 2 hr, and 1, 2, 3, and 6 days after unloading. The following activities were mea sured: adhesion receptor (CD 18 and L-selectin) expression of neutrophils and monocytes, migration capacity and percentage of apoptotic cells of neutrophils, serum soluble L-selectin (sL-selectin), plasma cortisol, and SCC. A significant increase in plasma cortisol and milk SCC was observed in TG. Leukocytosis, derived from neutrophils was recorded in TG, and was indicated by apoptotic measurement as an increase of young cells from the marginal pool. Increased migration and decreased surface expression of both L-selectin and CD 18 in neutrophils were observed after transportation. Elevated serum sL-selectin was also noted as a result of transportation. The present study indicated that transport stress modulates peripheral blood neutrophil function, particularly enhancing migration capacity, and c auses diapedesis across the mammary epithelium. Increased milk SCC in transported cattle might be due to these phenomena, and severe physiological stress may bring about an increase in SCC in milk.

Abstract. Human genetic studies have suggested that kisspeptin and neurokinin B (NKB) play pivotal roles in the control of gonadotropin-releasing hormone (GnRH) secretion. However, the role of NKB in this context is less clear compared with that of kisspeptin. In the present study, we investigated the ratio of colocalization of kisspeptin and NKB in neurons in the arcuate nucleus (ARC), the effects of intracerebroventricular infusion of NKB on luteinizing hormone (LH) secretion and whether the treatment activates ARC kisspeptin/NKB neurons in seasonally anestrous ewes. Double-labeling immunohistochemistry revealed that the majority of kisspeptin neurons coexpressed NKB in the ARC. Infusion of NKB for 2 h into the lateral ventricle elicited a discharge of LH, which resulted in significant increases in LH concentrations between 20 and 50 min after the start of infusion compared with a saline-infused control. Animals were sacrificed immediately after the end of infusion, and Fos expression in ARC kisspeptin neurons was immunohistochemically examined. The NKB treatment activated kisspeptin neurons throughout the ARC, and approximately 70% of kisspeptin neurons expressed Fos immunoreactivity at the caudal portion of the nucleus. The present study demonstrated that a central infusion of NKB elicited a discharge of LH, which was associated with the activation of a large population of ARC kisspeptin/NKB neurons in seasonally anestrous ewes. The results suggest that NKB plays a stimulatory role in the control of pulsatile GnRH secretion and that the population of ARC kisspeptin/NKB neurons is one of sites of the NKB action in sheep. Key words: Gonadotropin-releasing hormone, Kisspeptin, Neurokinin B, Seasonal anestrus, Sheep (J. Reprod. Dev. 58: [700][701][702][703][704][705][706] 2012) I nactivating mutations of not only Kiss1R, which encodes the kisspeptin receptor (GPR54), but also Tac3 and Tacr3, which encode neurokinin B (NKB) and its receptor (NK3R), respectively, produce gonadotropin deficiency and pubertal failure in humans [1][2][3][4]. These studies document that kisspeptin and NKB signaling play pivotal roles in the control of gonadotropin-releasing hormone (GnRH) secretion. Growing evidence indicates that kisspeptin acts as a potent stimulator of GnRH secretion in a variety of species [5], whereas the physiological role of NKB in this context is less clear.Human genetic studies [3,4] suggest that NKB would act to stimulate pulsatile GnRH/luteinizing hormone (LH) secretion.Indeed, it was demonstrated that a bolus intravenous (iv) injection of NKB or an agonist of NK3R, senktide, elicited a distinct LH discharge in castrated juvenile monkeys [6]. We also showed that a bolus intracerebroventricular (icv) administration of NKB induced a distinct LH pulse in ovariectomized (OVX) goats treated with estradiol (E2) and progesterone (P) [7]. However, in the goat study, the same treatment resulted in an overall reduction in LH secretion in the absence of gonadal steroids. A similar inhibitory effect of senktide was ...

Growth hormone (GH) secretion regularity and the effects of lighting condition and GH-releasing hormone (GHRH) on GH release were determined in steers. First, steers were kept under 12:12 L : D conditions (light: 06.00-18.00 hours). The animals were then subjected to a 1-h advancement in lighting on/off conditions (05.00 and 17.00 hours, respectively). Blood was sampled for 24 h at 1-h interval on the seventh day of each condition. Second, GHRH was injected intravenously (IV) at 12.00 and 00.00 hours under 12:12 L : D and blood was sampled at 15-min interval for 4-h (1 h before and 3 h after the injection). Plasma GH concentrations were measured by a radioimmunoassay. Periodicity of GH secretory profile was calculated by power spectrum analysis using the maximum entropy method. Plasma GH concentrations showed a characteristic pattern consisting of four distinct peaks. Mean periodicity of GH secretory profile was 5.7 h, and it was not altered by any change in lighting conditions. IV injection of GHRH increased GH secretion during the day and night. The increase in GH secretory volume after GHRH injection during the night was equal to that during the day. The present results suggest that GH secreted from the anterior pituitary have regularity in steers.

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ABSTRACT. The effects of melatonin (MEL) injection into the third ventricle (3V) on growth hormone (GH) secretion were investigated in conscious Holstein steers. A stainless steel cannula was stereotaxically implanted in the 3V based on the ventriculogram. In Exp. 1, three doses of MEL (100, 300 or 600 µg) were injected into the 3V through the cannula and the GH concentration after the injection was determined. In Exp. 2, intracerebroventricular (icv) and intravenous (iv) injections of MEL (100 µg) and GH-releasing hormone (GHRH; 0.25 µg/kg body weight), respectively, were performed simultaneously to examine the effect of MEL on GHRH-induced GH release. The icv injection of MEL significantly stimulated GH release at 100 µg. The increase in GH concentrations by 100 µg of MEL was persistent. Intravenous injection of GHRH dramatically increased GH release. The injection of MEL did not alter GHRH-induced GH release. These results suggest that MEL stimulates GH secretion possibly through the hypothalamus in cattle. KEY WORDS: cattle, melatonin, somatotropic axis, stereotaxic, third ventricle.J. Vet. Med. Sci. 68(10): 1075-1080, 2006 Growth hormone (GH) is a very important factor for livestock production [6]. GH-releasing hormone (GHRH) and somatostatin (SS) from the hypothalamus are primary factors controlling GH secretion in mammals. In addition to GHRH and SS, many neuromodulators have been considered to be involved in GH release regulation in many species. Although the central regulatory mechanism of GH secretion has been studied in sheep using hypophyseal portal blood sampling technique [4], such information is not well obtained in cattle.The evidences have shown the possibility that melatonin (MEL) from the pineal gland is one of those factors controlling GH secretion; however, the exact effect of MEL on GH secretion is controversial. For example, in humans it was reported that MEL induced an increase in GH levels [27,29]; however, other groups obtained no effects of MEL on GH secretion [13,31]. The intramuscular injection of MEL decreased GH secretion in prepubertal boys and the same dose of MEL increased GH level in some pubertal subjects [17]. In vitro experiments showed that MEL reduced GH secretion from rat pituitary cells [8]. These variations of the effects of MEL on GH secretion could be caused by the differences in the experimental and physiological conditions, and there might be inter-species differences regarding the role of MEL in the regulation of GH secretion.The purpose of the present study was to determine the role of MEL in the regulatory system of GH secretion in cattle. Since MEL has been reported to stimulate GH release via the hypothalamus [23,29], the technique for the direct injection of MEL into the third ventricle (3V) at three doses (100, 300 and 600 µg) was used. We also assessed whether MEL affects GHRH-induced GH release to reveal the involvement of the hypothalamus in GH secretion modulated by MEL. MATERIALS AND METHODS Animals:Eleven Holstein steers (7 to 8 mo old at the time of su...

To clarify the role of serotonin (5-HT) in the regulatory mechanism of L-tryptophan (TRP)--induced growth hormone (GH) secretion in cattle, changes in 5-HT concentrations in the cerebrospinal fluid (CSF) in the third ventricle (3V) and GH in plasma before and after the peripheral infusion of TRP were determined simultaneously. The direct effect of TRP on GH release from the dispersed anterior pituitary cells was also assessed. A chronic cannula was placed in 3V by stereotaxic surgery, then CSF and blood were withdrawn under physiological conditions. TRP (38.5 mg/kg BW) was infused through an intravenous catheter from 12.00 to 14.00 hours and CSF and blood sampling were performed from 11.00 to 18.00 hours at 1-h intervals. The concentration of 5-HT in CSF was determined by high-performance liquid chromatography with electrochemical detection. GH, melatonin (MEL), and cortisol (CORT) concentrations were measured by radio-immunoassay and enzyme-immunoassay. Concentrations of 5-HT were increased by TRP infusion. The TRP infusion significantly increased GH release. On the other hand, TRP did not stimulate GH release from the bovine pituitary cells. MEL and CORT concentrations were not altered by TRP infusion. These results suggest that TRP induced GH release via the activation of serotonergic neurons in cattle.

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