Surge Period Research Articles

Changes in the Messenger RNA Expressions of the Endothelin-1 and Angiotensin Systems in Mature Follicles of the Superovulated Bovine Ovary

The aim of the present study was to examine the messenger RNA expressions of the endothelin and angiotensin systems during the periovulatory phase in gonadotrophin releasing hormone (GnRH)-treated cows. Ovaries were collected by transvaginal ovariectomy (n=5 cows/group), and the follicles (n=5, one follicle/cow) were classified into the following groups: before GnRH administration (control, before LH surge), 3-5 h after GnRH (during LH surge), 10 h after GnRH; 20 h after GnRH, 25 h after GnRH (peri-ovulation), and early corpus luteum (CL) (Days 2-3). Expression of mRNA was investigated using quantitative real-time PCR. The expression of angiotensin converting enzyme (ACE) mRNA significantly decreased immediately after onset of the LH surge and remained at low levels. The levels of angiotensin II receptor type 1 (AT1R) and type 2 (AT2R) expression during the periovulatory period significantly decreased compared with other periods. The concentration of angiotensin II in follicular fluid began to increase 10 h after GnRH treatment and further increased as ovulation approached. The level of ET-1 mRNA significantly decreased 10 h after GnRH treatment compared with the levels before GnRH treatment and those of the early CL period. The expression of ETR-A and ETR-B mRNA during the periovulatory period were lower than in other periods. The expression of ECE-1 mRNA began to decrease in the LH surge period and significantly decrease in the periovulatory period compared with other periods. These results suggest that the vasoactive peptides angiotensin and endothelin may be associated with final maturation of follicles.

Antihypertensive Efficacy of Olmesartan Medoxomil and Candesartan Cilexetil in Achieving 24-Hour Blood Pressure Reductions and Ambulatory Blood Pressure Goals

For patients with hypertension, effective 24-hour blood pressure (BP) control is vital to ensure protection against the early morning surge in BP and the associated increased risk of cardiovascular events. The aim of this analysis was to assess the 24-hour antihypertensive efficacy of olmesartan medoxomil (20mg once daily) compared with candesartan cilexetil (8mg once daily), with particular emphasis on BP control during the early morning period. This is an additional analysis of a previously reported randomised, double-blind study in which 635 patients with mainly mild to moderate hypertension were randomised to 8 weeks of treatment with either olmesartan medoxomil 20 mg/day or candesartan cilexetil 8 mg/day. Changes from baseline during the last 4 and 2 hours of ambulatory BP measurement (ABPM) after 1, 2 and 8 weeks of treatment were compared between the two groups. In addition, the proportions of patients who achieved various ABPM goals, including those suggested by the European Society of Hypertension/European Society of Cardiology (ESH/ESC) [<125/80mm Hg] and the Japanese Society of Hypertension (JSH) [<135/80mm Hg], over 24 hours, during the daytime and at the last 4 and 2 hours of ABPM measurement were also compared. After 8 weeks, significantly greater proportions of patients treated with olmesartan medoxomil 20mg achieved 24-hour and daytime ABPM goals recommended by the guidelines of the ESH/ESC (25.6% and 18.3%, respectively) and JSH (37.5% and 26.6%, respectively) compared with candesartan cilexetil 8mg (24-hour ESH/ESC goal = 14.9%, p < 0.001; 24-hour JSH goal = 26.6%, p = 0.003; daytime ESH/ESC goal = 9.6%, p = 0.002; daytime JSH goal = 16.4%, p = 0.002). During the last 4 hours of 24-hour ABPM, the proportions of patients who achieved the ESH/ESC and JSH ABPM goals were significantly greater with olmesartan medoxomil (33.3% and 39.1%, respectively) than with candesartan cilexetil (22.9%, p < 0.001 and 31.6%, p = 0.047, respectively). Similarly, during the last 2 hours of 24-hour ABPM, the proportions of patients who achieved these BP goals were either significantly greater (JSH) or approached statistical significance (ESH/ESC) with olmesartan medoxomil (26.9% and 19.9%, respectively) compared with candesartan cilexetil (19.6%, p = 0.028 and 14.3%, p = 0.061, respectively). Compared with candesartan cilexetil 8mg, greater proportions of olmesartan medoxomil-treated patients (20mg) achieved ESH/ESC and JSH ABPM goals over 24 hours. The superior BP control of olmesartan medoxomil was also reflected in the larger proportions of olmesartan medoxomil-treated patients who achieved the ESH/ESC and JSH ABPM goals during the early morning surge period. This not only demonstrates that olmesartan medoxomil 20mg provides superior 24-hour BP reduction, but also suggests that olmesartan medoxomil may provide greater protection against the increased risk of cardiovascular events associated with the early morning BP surge period.

Southerly Surges on Submonthly Time Scales over the Eastern Indian Ocean during the Southern Hemisphere Winter

Abstract Meridional wind surges from the extratropics into the Tropics strongly regulate tropical convective activity. This paper confirms that extratropical forcing manifested as a meridional surge does modulate the tropical atmosphere over the eastern Indian Ocean, and it describes the tropical–extratropical connection in the region. Surges in the lower atmosphere on submonthly (6–25 days) time scales over the eastern Indian Ocean were examined in tandem with associated tropical convection and large-scale atmospheric fields during the Southern Hemisphere (SH) winter (June–August). Data used in this study are NCEP-2 reanalyses and daily NOAA/Climate Diagnostics Center (CDC) outgoing longwave radiation (OLR) data for 23 yr, from 1979 to 2001. A low-level surge index was calculated using the 850-hPa meridional wind component (υ) averaged over a region where sub–monthly scale υ variance shows a local maximum (17.5°–2.5°S, 87.5°–97.5°E). The surge index defines 62 different surge events. Composites of various components were generated based on the index to define relationships between surge events and large-scale fields. Low-level southerly surges over the eastern Indian Ocean originate from midlatitude Rossby waves with strong baroclinic development in the entrance region of a subtropical jet core off Australia’s west coast. Strengthened low-level wind surges cause cross-equatorial flow stretching from the subtropical eastern Indian Ocean to the southern Bay of Bengal. Surges are accompanied by the advection of cold, dry air from midlatitudes into the Tropics. A cold and dry front develops at the leading surge edge during the surge period. Two to four days later, as the surge peaks, negative OLR anomalies develop near the key region. The OLR anomalies indicate a local blow up of convection over the tropical eastern Indian Ocean. Convection reflects increased instability in the surge region, which is caused by low-level dry air advection and near-surface moistening that is forced by enhanced sea surface evaporation associated with the surge. The southerly surge on submonthly time scales is an important bridge linking the Tropics and midlatitudes over the Indian Ocean.

Temporal variations in flow velocity at Finsterwalderbreen, a Svalbard surge-type glacier

AbstractInter- and intra-annual velocity variations are well known on alpine glaciers, but their importance for Arctic glaciers has only been recognized more recently. This paper presents flow velocity data from Finsterwalderbreen, a 35 km2 polythermal surge-type glacier in southern Svalbard that is presently ∼100 years into its quiescent phase. Field measurements of glacier surface velocities are available from 1950-52 and 1994-97, and mean velocities for the last decade are estimated for the lower glacier using cables drilled to the glacier bed. These velocities show substantial seasonal variations indicating that basal sliding is an important component of surface velocities and interannual fluctuations of up to 75%, possibly indicating variations in subglacial water storage. Several lines of evidence indicate that this glacier has an extensive subglacial hydrological system, generally considered to be a prerequisite for surge-type glaciers, which is at least partly pressurized. Information on surface morphology from 1898 onwards shows that the glacier has experienced continuous retreat since the last surge in about 1910, and has now retreated ∼1.5 km further back than its previous pre-surge position in 1898. Tracking of moraine loops on terrestrial and aerial photographs acquired over a 100 year period indicates that the surge period of Finsterwalderbreen may be lengthening in response to climate changes.

Involvement of opioid receptor subtypes in both stimulatory and inhibitory effects of the opioid peptides on prolactin secretion during pregnancy.

1. We have previously demonstrated the existence of a dual neuromodulatory regulation of prolactin secretion by the opioid system. In the present work, we evaluated the opioid receptor subtypes involved in both the stimulatory and the inhibitory regulation of prolactin secretion in pregnant rats. 2. Specific opioid agonists and antagonists were administered intracerebro ventricular (i.c.v.) to rats on day 3 and on day 19 pregnancy in rats of pretreated with mifepristone. Blood samples were obtained after decapitation at 12.00 and 18.00 h. Serum prolactin levels were measured by RIA. 3. The mu-selective agonist DAMGO and beta-endorphin caused a significant increase in serum prolactin secretion on day 3 of pregnancy, during the diurnal surge and intersurge period. Pretreatment with naloxone prevented the increase on prolactin levels induced by DAMGO. The administration of U-50,488, a kappa-selective agonist or DPDPE, a delta-selective agonist, did not modify serum prolactin concentration while the mu1-antagonist naloxonazine reduced significantly serum prolactin levels. On day 19 of pregnancy, the release of prolactin induced by mifepristone was significantly increase by naloxonazine, while the kappa-antagonist nor-binaltorfimine induced only a small but significant increase. No effect was observed after administration of the delta-antagonist naltrindole. 4. We conclude that the mu-opioid receptor seems to be more specifically involved in both the stimulatory and inhibitory regulation by the opioid system on prolactin secretion during pregnancy. The increase on serum prolactin levels on day 3 after administration of DAMGO and beta-endorphin may suggest the participation of other regulatory mechanisms as the dopaminergic and serotoninergic systems. On day 19, only the endogenous ligands delta did not participate in the regulation of prolactin secretion, while the participation of the kappa-opioid receptor was significantly less effective than the endogenous ligand mu. Our results provide evidences of an important role of the opioid system through specific receptors on the regulation of prolactin secretion during early and late pregnancy.

Dynamic expression of p38β MAPK in neurons and astrocytes after transient focal ischemia

Here we report the dynamically regulated expression of p38β MAPK isoform in specific subsets of cells in postischemic brain. The activity of p38β MAPK in the postischemic brain revealed biphasic induction at 30 min and 4 days after 1 h MCAO. During the early surge period, p38β MAPK was preferentially localized in the nucleus and dendrites of neurons in the future infarction area, while during the delayed surge p38β MAPK was heavily induced in reactive astrocytes in penumbra. The temporally and spatially regulated pattern of p38β MAPK expression in the postischemic brain suggests distinct roles of p38β MAPK in neuronal death and in the astrocyte activation.

Periovulatory changes in the local release of vasoactive peptides, prostaglandin f(2alpha), and steroid hormones from bovine mature follicles in vivo.

We previously proposed that an endothelin-angiotensin-atrial natriuretic peptide system may contribute to inducing ovulation of mature bovine follicles by modulating follicular secretion of steroids and prostaglandins (PGs). Thus, this study aimed to determine the real-time changes in the local release of angiotensin II (Ang II), endothelin (ET), atrial natriuretic peptide (ANP), PGF(2alpha), and steroid hormones from bovine mature follicles during the periovulatory period in vivo. Seven cows were treated for superovulation using FSH and PGF(2alpha) injections. Two dialysis capillary membranes per follicle were surgically implanted into the theca layer of mature follicles and connected to a microdialysis system (MDS). Fractions of the perfusate were collected from Day -1 (Day 0 = LH surge) to Day 3. Five out of seven treated cows were normally ovulated, and the newly formed corpora lutea were observed at the end of the experiment. In these five ovulated cows, the release of estradiol, androstenedione, and progesterone in the theca layer increased (P < 0.05) synchronously with the LH surge. Acute increases in PGF(2alpha) and Ang II concentrations in the ovarian venous plasma (OVP) were observed at 24-48 h after the peak of the LH surge, when multiple ovulations were expected to occur. The follicular Ang II release was low during the pre-LH surge period and rose (P < 0.05) at the beginning of the increase in the LH surge. On the other hand, ET-1 release dropped (P < 0.05) when plasma LH started to increase. However, no clear changes in ANP concentration in the MDS perfusate and plasma were observed. The above local changes in Ang II, PGF(2alpha), as well as steroid hormones were not observed in cows (n = 2) that did not show an LH surge and ovulation. The present results demonstrate for the first time the local release of Ang II, ET-1, and ANP from the bovine mature follicle in real-time in vivo and show that Ang II and PGF(2alpha) concentrations in the OVP acutely increase around the time of ovulation. The overall results support the concept of a local functional ET-Ang-ANP system in the bovine mature follicle that may be involved in the ovulatory process.

99/00561 Hydrogen formation from biomass using solar energy

An intense field observation was carried out for a better understanding of cold surge features over Peninsular Malaysia during the winter monsoon season. The study utilizes vertical profiles of temperature, humidity and wind at high vertical and temporal resolution over Kota Bharu, situated in the east coast of Peninsular Malaysia. LCL were elevated during the passage of the cold surge as the relative humidity values decreased during the passage of cold surge. Level of Free Convection were below 800 hPa and equilibrium levels were close to the LFC in most of the cases. Convective available potential energy and convection inhibition energy values were small during most of the observations. Absence of local heating and instability mechanism are responsible for the peculiar thermodynamic structure during the passage of the cold surge. The wind in the lower atmosphere became northeasterly and was strong during the entire cold surge period. A slight increase in temperature near the surface and a drop in temperature just above the surface were marked by the passage of the cold surge. A remarkable increase in specific humidity was observed between 970 and 900 hPa during the cold surge period. Further, synoptic scale features were analyzed to identify the mechanism responsible for heavy rainfall. Low level convergence, upper level divergence and cyclonic vorticity prevailed over the region during the heavy rainfall event. Dynamic structure of the atmosphere as part of the organized convection associated with the winter monsoon was responsible for the vertical lifting and subsequent rainfall.

Estradiol-Dependency of Sexual Behavior Manifestation at the Post-LH Surge Period in Ovariectomized Goat.

This study was conducted to examine whether or not the post-luteinizing hormone (LH) surge termination of estrus could be delayed by prolonged exposure to estradiol. Subcutaneous tubings containing estradiol were implanted in eight ovariectomized goats to maintain blood estradiol at the follicular phase level for 56-80 h. Behavior observation and blood sampling were carried out every 2 h for 114 h from 6 h before through 108 h after the initiation of estradiol treatment. As a result, the duration of proceptivity (defined as an active approach to the male) and receptivity (defined as an acceptance of the male) were extended in the manner reflecting the length of estradiol administration. The proceptivity and receptivity disappeared at 14.5 ± 5.0 h and 8.0 ± 3.6 h (mean ± SEM, n=8) after the removal of estradiol tubings, respectively. These results suggest that the termination of estrus in female goat is due to a decline of circulating estradiol level following the LH surge, and that the central nervous system regulating behavioral estrus maintains its responsiveness to estradiol even at the post-LH surge period.

Simultaneous measurement of gonadotropin-releasing hormone in the third ventricular cerebrospinal fluid and hypophyseal portal blood of the ewe.

GnRH is present in the hypophyseal portal blood and cerebrospinal fluid (CSF) of several species investigated, including sheep, but the precise relationship between these two compartments of GnRH is unknown. In the present study, ovariectomized steroid-treated ewes were surgically prepared for the simultaneous collection of portal blood and third ventricular CSF. Ten-minute samples were collected for pulse analysis after progesterone removal and hourly for comparisons during the estradiol-induced LH surge. The time of onset of the portal (15.3 +/- 0.5 h after estradiol) and CSF (15.9 +/- 0.2 h) GnRH surges was similar and occurred coincidentally with the LH surge (15.6 +/- 0.4 h). The period of the surge during which GnRH concentrations exceeded half-maximal levels (portal, 7.3 +/- 1.5 h; CSF, 7.3 +/- 0.3 h) was the same and outlasted the corresponding LH surge period (3.3 +/- 0.3 h). LH pulses started and peaked later than the corresponding portal GnRH pulses (onset difference, 10 +/- 1 min; peak difference, 16 +/- 1 min; P < 0.01 for both), but the times of pulse onset and peak were not significantly different from those of concomitant CSF GnRH pulses (onset difference, 8 +/- 6 min; peak difference, 8 +/- 4 min). Although the times of pulse onset and peak did not differ between the portal and CSF GnRH compartments (onset difference, 4 +/- 6 min; peak difference, 6 +/- 2 min), CSF GnRH pulses were longer than their portal counterparts (CSF, 38 +/- 3 min; portal, 15 +/- 1 min; P < 0.01). The amplitude of jugular LH pulses was strongly correlated (r2 = 0.85) with portal GnRH pulse amplitude, but not with that of CSF GnRH pulses (r2 = 0.45); there was no correlation between portal and CSF GnRH pulse amplitudes (r2 = 0.25). These data show that third ventricular CSF GnRH reliably relates neurosecretory events occurring within the hypophyseal portal system at the time of the preovulatory LH surge, but is not as precise as portal GnRH in marking a LH pulse.

Inhibition of the LH surge in cyclic rats by stress is not mediated by opioids.

The effects of intravenous (iv) administration of the opioid antagonists naloxone and naltrexone on the restraint-induced suppression of the pro-estrous LH surge were studied in cyclic female rats. To minimize stress during repeated blood sampling, the rats were provided with a jugular vein cannula. Restraint stress for 6 hrs starting at t = -1 h (the onset of the LH surge being at t = 0 h) caused a suppression of LH levels (including peak height) during the period of the LH surge. Repeated naloxone injections, given 3 h (1 mg), 4 h (0.5 mg) and 5 h (0.5 mg) after the onset of the LH surge, did not affect the restraint-induced inhibition neither did pretreatment with 1 mg naloxone at t = -75 min (i.e. 15 min before application of restraint). Naltrexone (2 mg) administered at t = -15 min induced higher plasma LH levels at t = -6 min. When rats were subsequently subjected to restraint for 5 hrs starting at t = -5 min, the restraint-induced inhibition of surge levels of LH was not affected. The results indicate that withdrawal of opioid activity in cyclic female rats before the presumed onset of the LH surge results in a premature rise of LH levels. This is in accordance with the notion that LH levels prior to the surge are under tonic inhibition of endogenous opioid peptides (EOP). In addition, the data show that opioid receptor antagonism during or before application of restraint does not alter the restraint-induced suppression of the LH surge. It is therefore concluded that EOP do not mediate the inhibitory effect of restraint stress on the LH surge in cyclic rats.

Actively surging West Antarctic ice streams and their response characteristics

Ice Streams B, D and E, West Antarctica, all show a longitudinal pattern of ice thickness change that is consistent with ongoing surge behavior modeled for glaciers. The measured pattern is not consistent with model response of any other scenario such as accumulation-rate change or changes on the ice shelf. Inland migration of the ice-stream onset is a requirement of this behavior pattern. If such a surge is presently taking place, the remaining lifetime of the West Antarctic ice sheet is 1200–6000 years. A complete surge period lasting 50 000–120 000 years is hypothesized, with a relatively brief surge phase (lasting 16000–21 000 years) required to completely remove the West Antarctic ice sheet from its maximum extent. Applying classic glacier response theory demonstrates that the diffusive component of response is much faster for ice streams than for glaciers, making the identification of either kinematic waves or localized responses on ice streams unlikely.

Actively surging West Antarctic ice streams and their response characteristics

Ice Streams B, D and E, West Antarctica, all show a longitudinal pattern of ice thickness change that is consistent with ongoing surge behavior modeled for glaciers. The measured pattern is not consistent with model response of any other scenario such as accumulation-rate change or changes on the ice shelf. Inland migration of the ice-stream onset is a requirement of this behavior pattern. If such a surge is presently taking place, the remaining lifetime of the West Antarctic ice sheet is 1200–6000 years. A complete surge period lasting 50 000–120 000 years is hypothesized, with a relatively brief surge phase (lasting 16000–21 000 years) required to completely remove the West Antarctic ice sheet from its maximum extent. Applying classic glacier response theory demonstrates that the diffusive component of response is much faster for ice streams than for glaciers, making the identification of either kinematic waves or localized responses on ice streams unlikely.

Effect of intravenous or intracerebroventricular injections of His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 on GH release in conscious, freely moving male rats.

The present study was designed to examine the effects of intracerebroventricular injection of His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP) on GH secretion in freely moving conscious male rats and to determine whether the central action of GHRP is mediated by increased GHRH and/or somatostatin (SRIF) release. A significant and dose-related suppression of natural fluctuations in plasma GH occurred immediately after intracerebroventricular injection of GHRP at the doses of 1, 3 and 10 mu g/rat and was sustained for more than 1 h. An intracerebroventricular injection of GHRP also suppressed plasma GH rises after an intravenous injection of [D-Ala2, Nle27] human GHRH (1-28)agmatine (hGHRH analog), but the GH suppression by intracerebroventricular GHRP was significantly blunted in rats treated with antirat SRIF gamma-globulin (SRIF-ab). In addition, the suppression by intracerebroventricular GHRP of hGHRH-analog-induced GH release was observed even in rats treated with anti-rat GHRH goat gamma-globulin (GHRH-ab) which does not cross-react with hGHRH analog, and again its suppression was significantly attenuated by simultaneous treatment with SRIF-ab and GHRH-ab. Furthermore, intracerebroventricularly injected GHRP was effective enough to inhibit the central-nervous-system (endogenous GHRH)-driven natural GH-secretory surges in SRIF-ab-treated rats. When 10 mu g/kg GHRP was injected intravenously every 1 h during a 7-hour observation period in control rats without antibody treatment, plasma GH levels were increased with the peak 10 min after each injection during the surge period of the GH-secretory rhythm, but the plasma GH response to GHRP was frequently absent during its trough period. In addition, in SRIF-ab-treated rats, basal GH levels as well as plasma GH peaks after GHRP injections were markedly elevated and the obvious plasma GH rises after GHRP could be observed even during the trough period. In GHRH-ab-treated rats, basal GH levels were lower, and the plasma GH response to GHRP was significantly attenuated as compared with those in control rats. Plasma GH peaks after GHRP injections in rats simultaneously treated with SRIF-ab and GHRH-ab were higher than those in rats given GHRH-ab alone, but its difference in GH response was obviously smaller than that observed between SRIF-ab-treated and control rats, suggesting a crucial role of endogenous GHRH in GHRP-induced GH release. To further clarify the interaction of GHRH and GHRP in GH release, hGHRH analog was injected intravenously alone or simultaneously with GHRP in rats treated with SRIF-ab and GHRH-ab. The peak GH values after simultaneous injection of hGHRH analog and GHRP were significantly higher than the sum of GH peaks after each injection of hGHRH analog and GHRP. In conclusion, an intracerebroventricular injection of GHRP suppresses GH secretion by a central mechanism which is likely to include increased SRIF release, reduced GHRH release or both. We have confirmed that intravenous injection of GHRP can stimulate GH release by itself in an immunologically nullified condition of circulating endogenous GHRH and SRIF in rats, and that endogenous SRIF modestly suppresses the GH-stimulating effect of intravenously injected GHRP while both endogenous and exogenous GHRH markedly enhance GH release by intravenously injected GHRP in a synergistic manner.

Semicircadian rhythm of dopamine release in the mediobasal hypothalamus in awake rats during pseudopregnancy: evidence that a thyrotropin-releasing hormone analogue stimulates dopamine release and thereby inhibits prolactin secretion.

The release of dopamine (DA) from tuberoinfundibular (TIDA) neurons during prolactin (PRL) surge and nonsurge periods and the effects of the thyrotropin-releasing hormone (TRH) analogue CG 3703 on DA and PRL secretion were studied in awake pseudopregnant (PSP) rats by simultaneous measurement of extracellular DA levels in the mediobasal hypothalamus (MBH) by means of microdialysis and of plasma PRL concentrations by radioimmunoassay of PRL in blood sampled from a permanent heart cannula. Since basal DA levels were low, the experiments were performed under local infusion of the reuptake inhibitor nomifensine (5 mumol/l), which increased extracellular DA levels 5-fold around the probe, but did not affect the occurrence of the nocturnal PRL surge on day 7-8 of PSP. Under nomifensine conditions, during the interphase (18.00-1.00 h) plasma PRL levels were low (< 50 ng/ml), while the DA release from TIDA neurons was elevated (approximately 250%) relative to the DA values measured during the phase when the nocturnal PRL surge occurred (100%; 1.00-12.00 h; plasma PRL levels were elevated to approximately 300 ng/ml). Thus, semicircadian rhythms were detected both for DA and PRL, which were broadly reciprocal in timing. The TRH analogue CG 3703 (100 and 500 micrograms/animal i.v.), when administered at 00.00 h, dose-dependently increased extracellular DA levels (to 300 and 500% of pretreatment values, respectively) and postponed the PRL surge in a corresponding manner (for approximately 2 and 3 h, respectively). Thus, in addition to its PRL-releasing effects, TRH can also suppress the PRL secretion by stimulating the release of DA from TIDA neurons, thereby increasing the inhibitor DAergic tone on lactotrophs. During the interphase, when DA levels were relatively elevated, administration of the DA blocking agent HA 966 (100 mg/kg body weight i.p.) at 20.00 h resulted in a short-lasting decrease in extracellular DA levels (to approximately 60% of pretreatment values for 30 min) accompanied by an immediate, short-lasting increase in PRL levels (to 400 ng/ml for approximately 1 h). Administration of CG 3703 (500 micrograms/animal i.v.) in combination with HA 966 (100 mg/kg body weight i.p.) at 20.00 h prevented the decrease in DA levels and the rise in plasma PRL values. Thus, the TRH analogue and HA 966 counteracted each other regarding the DAergic system, which again illustrates the stimulatory effect of the TRH analogue on the release of DA from TIDA neurons. Moreover, our results suggest that the interphase and the phase during which the nocturnal PRL surge occurs under the condition of PSP differ with regard to the DAergic inhibition of the PRL secretion; during the interphase the DAergic inhibitory tone prevents the rise in PRL secretion, while during the nocturnal PRL surge period another factor in addition to a decrease in DA levels appears necessary to increase plasma PRL levels.

A Simple Model for Current Speed in Tidal Channels

Danish Journal of Geography 95: 12–18, 1995. A simple model for current speed in tidal channels is presented and tested in a tidal channel in the Danish Wadden Sea. The model is based on the continuity equation with water level as the only time dependant input parameter. The model can be used as a tool for extending and/or completing current speed time series in tidal channels. In four test periods the model proved to be able to explain over 95% of the current speed variation during periods with “normal” wind conditions, and 91% of the variation during a tested storm surge period.

Differential effects of estrogen and progesterone on levels of POMC mRNA levels in the arcuate nucleus: relationship to the timing of LH surge release.

Beta-endorphin is thought to be an important inhibitor of LHRH neuronal activity and also to play a role in conveying information about changes in steroid levels to LHRH neurons. We have previously shown that the mRNA encoding the precursor of beta-endorphin, proopiomelanocortin (POMC), fluctuates during the estrous cycle with the most dramatic changes occurring on proestrus. POMC mRNA levels decline before the onset of LH surge release but then dramatically rise and remain elevated during the surge. In the present studies we tested the hypothesis that the decline in POMC mRNA levels immediately before the proestrus LH surge is mediated by estrogen and the rise during the surge by progesterone. To test this hypothesis, we compared changes in POMC mRNA levels between ovariectomized (OVX) and OVX estrogen (E2)-treated rats and between OVX E2-treated rats with and without progesterone. Animals were examined at hourly intervals after the administration of progesterone, then at every 4 h during the LH surge. Using in situ hybridization histochemistry, we found that E2 decreased POMC mRNA levels in OVX rats before the onset of the LH surge and further suppressed levels during the surge. Compared to animals treated with E2 alone, progesterone advanced the time at which both the LH surge began and the time at which POMC mRNA levels declined. After a transient decline, POMC mRNA levels rose in these progesterone-treated animals and remained elevated throughout the period of the LH surge. These results support the hypothesis that progesterone times the LH surge and limits its appearance to one day be exerting a biphasic effect on the activity of beta-endorphinergic neurons of the arcuate nucleus.

Effect of naloxone and pulsatile luteinizing-hormone-releasing hormone infusions on oestradiol-induced luteinizing hormone surges in immature gilts

The aim of the study was to understand why immature 60-day-old gilts produce delayed low amplitude luteinizing hormone (LH) surges in response to oestradiol benzoate. In Expt 1, gilts (n = 36) were challenged with oestradiol benzoate and subsequently received either no further treatment or were infused with saline or various doses of the opioid antagonist, naloxone, for 6-48 h during the expected LH surge (48-96 h after oestradiol benzoate). No differences were observed among groups in the magnitude or duration of the LH surge. In contrast to the other groups, LH concentrations in gilts infused for 48 h with naloxone did not decrease after the surge period. In Expt 2, gilts (n = 34) were challenged with oestradiol benzoate or sesame oil and subsequently received pulses of luteinizing-hormone-releasing hormone (LHRH) or saline solution during the expected surge period. Two other groups were fed methallibure to pharmacologically suppress the oestradiol benzoate-induced LH surge. In addition, one of these groups was given pulses of an LHRH agonist (LHRH-A) during the surge period. Within 2 h of the start of pulsatile LHRH infusion, LH increased in sesame oil-treated gilts, but not in oestradiol benzoate-treated gilts, suggesting that the pituitary responsiveness to LHRH in immature gilts is decreased by oestrogen before the onset of the LH surge. Pulsatile LHRH infusion did not enhance the amplitude of oestradiol benzoate-induced LH surges nor did it advance its onset. Feeding methallibure suppressed the oestradiol benzoate-induced LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolonged suppression of serum concentrations of melatonin in prepubertal heifers.

Our objective was to suppress the daily surge of melatonin in serum of prepubertal dairy heifers by manipulating intensity of light (Experiment 1) and duration of exposure to light (Experiment 2). Heifers in Experiment 1 were exposed to either 12 hr of darkness (000 lux, control), or 400, 800, or 1,200 lux of light during the last 6 hr of their usual 12-hr nocturnal period. During this 6-hr exposure to various intensities of light, melatonin concentrations were similar to their respective daytime baseline values measured under 400 lux of light, but were 62% to 82% lower than melatonin concentrations during their nocturnal surge period. Suppression of melatonin concentrations was similar between 400 and 1,200 lux of light. In Experiment 2, heifers were exposed to LD 8:16, LD 16:8, LD 20:4, or LD 24:0 photoperiods (1,200 lux) for 4 months. Throughout treatment, concentrations and durations of the melatonin surge were suppressed in the LD 24:0 group and were greatest (during the nocturnal period) in the LD 8:16 group. Concentrations of prolactin in serum were elevated in animals under long days relative to LD 8:16 treatment and respective pretreatment periods. In conclusion, continuous light at an intensity of 1,200 lux suppressed the nocturnal surge of melatonin, but increased secretion of prolactin for at least 4 months in prepubertal heifers.

Effects of Photoperiod on Mammary Development and Concentration of Hormones in Serum of Pregnant Dairy Heifers

Beginning at 128 d of pregnancy, Holstein heifers were exposed to 16h light, 8h dark (long days; n = 10) or 8h light, 16h 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.