Rise In Release Research Articles

Endocrine basis for puberty in heifers and ewes

Maturation processes that culminate in puberty and sexual maturity are initiated before birth, continue through prepuberty (> 50 days before puberty) and peripuberty (50 days before puberty) and are completed early after puberty. The hypothalamus is the primary site of change during transition to sexual maturity. Maturation of the hypothalamus results from decreased negative feedback of oestradiol that leads to increased frequency of release of LH pulses. Increased tonic release of LH pulses during sexual maturation is the primary endocrine factor that regulates the onset of puberty in ewe lambs and heifers. Increased frequency of release of LH pulses enhances development of ovarian follicles which produce enough oestradiol to induce behavioural oestrus and a preovulatory surge of gonadotrophins. In later stages of peripuberty, ovulation or luteinization of follicles results in transient increases in progesterone for shorter periods than is typical for luteal phases of the oestrous cycle of mature ewes and cows. Transient increases in progesterone are not generally preceded by behavioural oestrus. After the demise of the transient luteal structures, puberty is attained with occurrence of the first behavioural oestrus that is accompanied by ovulation and development of a corpus luteum with a typical lifespan. At puberty, all components of the hypothalamic-pituitary-ovarian axis are in place for oestrous cycles to be expressed. Factors that can influence the pubertal rise in release of LH pulses are genotype, gender, season of year when pubertal age is attained, growth or nutritional intake, social cues or treatment with exogenous progestins. Sexual maturation continues after puberty with an enhanced probability of pregnancy occurring from actions of ovarian steroids at the uterus.

Adrenergic activation of melatonin secretion in ovine pineal explants in short-term superfusion culture occurs via protein synthesis independent and dependent phenomena.

The ovine pineal is generally considered as an interesting model for the study on adrenergic regulation of melatonin secretion due to some functional similarities with this gland in the human. The present investigations, performed in the superfusion culture of pineal explants, demonstrated that the norepinephrine-induced elevation of melatonin secretion in ovine pinealocytes comprised of two subsequent periods: a rapid increase phase and a slow increase phase. The first one included the quick rise in release of N-acetylserotonin and melatonin, occurring parallel to elevation of NE concentration in the medium surrounding explants. This rapid increase phase was not affected by inhibition of translation. The second, slow increase phase began after NE level had reached the maximum concentration in the culture medium and lasted about two hours. It was completely abolished by the treatment with translation inhibitors. The obtained results showed for the first time that the regulation of N-acetylserotonin synthesis in pinealocytes of some species like the sheep involves the on/off mechanism, which is completely independent of protein synthesis and works very fast. They provided strong evidence pointing to the need of revision of the current opinion that arylalkylamines N-acetyltransferase activity in pinealocytes is controlled exclusively by changes in enzyme abundance.

Ileal mucosal response to bacterial toxin challenge.

The cause of postinjury intestinal mucosal barrier disruption remains obscure. The present study examines the hypothesis that the bacterial toxin formyl-methionyl leucyl phenylalanine (FMLP) plays an initial role in this process. Mucosal permeability to fluorescein isothiocyanate-labeled dextran (4,400 molecular weight) was measured in perfused distal rat ileum with and without FMLP. Dextran and myeloperoxidase appearance in the lumenal perfusate was assessed in response to surrogates of traumatic stress: ischemia/reperfusion, total abdominal irradiation, and total parenteral nutrition. Recovery of FMLP in the effluent of static closed and perfused ileal loops was determined by mass spectrometry. Release of mast cell mediators in the presence of FMLP was determined in ileal everted sacs. Seventy-five percent of FMLP was recovered in perfusion effluent in contrast to 5% in closed loops. There was a transient increase in ileal permeability in FMLP/perfused, untreated rats, and in ischemia/reperfusion and total parenteral nutrition treated rats that was recorded with a concomitant increment in myeloperoxidase (inflammatory marker) in all experimental models except irradiated rats, which were unresponsive to FMLP. FMLP responsiveness was associ. ated with a significant rise in release of serotonin (mast cell mediator). These results suggest that mast cells and other resident inflammatory cells within the gut wall are involved in FMLP-induced changes in mucosal barrier permeability and raise the possibility that under conditions of traumatic stress, proinflammatory mediators within the gut wall might be activated by toxic factors in the gut lumen.

Interleukin 1-beta modulates the effects of hypoxia in neuronal culture

In order to study the role of interleukin-1beta (IL-1β) in homeostasis, hypoxia and recovery of neuronal cells, we studied the expression and release of tumor necrosis factor-alpha (TNF-α) and nerve growth factor (NGF), in relation to the presence or absence of this cytokine in culture medium. Moreover, we evaluated cell mortality in the same conditions. For this aim, we used untreated and IL-1β pre-immunoneutralized hippocampal neuronal cultures exposed to mild hypoxic stress and left to reoxygenate. Semiquantitative reverse-transciptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) determined gene expression and protein levels. Mild hypoxic stress provokes a decrease in both the expression and release of TNF-α and NGF. IL-1β neutralization results in an inversion of this pattern since treated hypoxic cultures exhibited an increase of both expression and release of NGF. In pretreated hypoxic cells the increased expression of TNF-α was not followed by a rise in release. Reoxygenation reversed the observed effects in both cultures and the levels of cytokine expression and release were approaching control values. Our data show that in physiological conditions IL-1β may have a neuroprotective action through positive modulation of NGF. Contrary to that, in presence of insult, IL-1β may have an opposite role, since neutralization provoked an increase of expression and release of NGF. In addition, we demonstrated that neuronal cells are biochemically capable, not only of maintaining and recovering the homeostasis, but also of activating the appropriate response to insult. IL-1β may have a pivotal role in this mechanism through the modulation of NGF and to a lesser degree of TNF-α.

Involvement of 5-Hydroxytryptamine, Prostaglandin E2, and Cyclic Adenosine Monophosphate in Cholera Toxin-Induced Fluid Secretion in the Small Intestine of the Rat In Vivo

The diarrhea of cholera is considered to rely solely on a cyclic adenosine monophosphate-mediated secretory mechanism. However, both 5-hydroxytryptamine and prostaglandin E2 have been proposed to be involved in the pathogenesis of cholera. In vivo experiments were performed, therefore, in the rat jejunum to investigate the influence of purified cholera toxin on fluid secretion, luminal release of 5-hydroxytryptamine and prostaglandin E2, and formation of mucosal cyclic adenosine monophosphate. Also the effects of ketanserin, indomethacin, verapamil, and nifedipine on the named parameters were studied. Cholera toxin dose-dependently (0.1-0.5 microgram/ml) and time-dependently (1-5 h) increased mean net fluid secretion with a maximum response at 4 h. It also caused a significant (p less than 0.01) rise in release of 5-hydroxytryptamine and prostaglandin E2, in addition to formation of cyclic adenosine monophosphate. The dose-response curve for cholera toxin-induced fluid secretion was shifted to the right by indomethacin (10 mg/kg s.c.) and ketanserin (200 micrograms/kg s.c.), none of which caused a change in cholera toxin-induced release of 5-hydroxytryptamine. However, both agents significantly decreased the release of prostaglandin E2. Verapamil (0.2-9.5 micrograms/min i.a.) and nifedipine (0.05-0.5 microgram/min i.a.) dose-dependently reduced cholera toxin-induced fluid secretion. The estimated local concentrations at half-maximal inhibition were 5 x 10(-7) M verapamil and 5 x 10(-8) M nifedipine, respectively. The cholera toxin-induced increase in release of 5-hydroxytryptamine and prostaglandin E2 and formation of cyclic adenosine monophosphate was unaffected by verapamil. These results support the concept that cholera toxin-induced fluid secretion in vivo is caused, in part, by release of 5-hydroxytryptamine, which in turn stimulates formation of prostaglandin E2.

Role of complement C9 and calcium in the generation of arachidonic acid and its metabolites from rat polymorphonuclear leukocytes

We have previously shown that antibody-sensitized mouse peritoneal macrophages release arachidonic acid (C20:4) and its oxygenated derivatives when treated with complement, and that the major part of the release depended on the terminal complement complexes (TCC). To further delineate the process(es) responsible for this release we have extended our studies to rat peritoneal poly-morphonuclear leukocytes (PMNs). Experiments were performed with antibody-sensitized rat PMNs labeled with [ 3H]C20:4 and carrying the TCC, C5b-7, C5b-8 or C5b-9. In contrast to the results of other studies, production of leukotriene B 4 (LTB 4), the major radiolabeled derivative, was strictly dependent on the presence of C9. However, low levels of C20:4 and prostaglandins (PGs) were produced prior to the C5b-9 stage. Kinetic studies demonstrated that release of LTB 4 was rapid; the initial release occurred within 4–6 min and a second rise in release coincided with cell death. Virtually all the LTB 4 produced was released as we found no evidence of retention of intracellular LTB 4 at either the C5b-8 or C5b-9 stages. In the absence of extracellular calcium, the release of LTB 4 was completely abolished and the release of C20:4 and PGs was drastically reduced. [ 3H]C20:4-labeled PMNs carrying C5b-9 did release substantial amounts of radiolabeled material in the presence of EGTA; however, the majority of this lipid was in the form of intact phospholipid and triglyceride. These results indicate that release of C20:4 and its oxygenated derivatives from rat PMNs is (1) dependent on the participation ofC9 in the preexisting C5b-8 complex in the cell membrane, and (2) largely dependent on the presence of calcium.

Somatostatin and altered medium osmotic pressure elicit rapid changes in prolactin release from the rostral pars distalis of the tilapia, Oreochromis mossambicus, in vitro

Prolactin (PRL) cells in the rostral pars distalis of the tilapia Oreochromis mossambicus respond to somatostatin (SRIF) and reduced medium osmotic pressure within 10–20 min of exposure during perifusion incubation. Pieces of rostral pars distalis tissue were removed from freshwater-adapted tilapia and were preincubated in [ 3H]leucine in static culture (355 mØsmolal) for 48 hr. Following preincubation, they were placed in the perifusion apparatus and baseline release was established for 3 hr in hyperosmotic medium (355 mØsmolal). Exposure to hyposmotic medium (280 mØsmolal) resulted in a rapid and steep rise in the release of [ 3H]PRL, which remained elevated for more than 2 hr. When SRIF was added simultaneously with hyposmotic medium, the rise in PRL release normally initiated by reduced osmotic pressure was prevented. Somatostatin also quickly reduced release that had been previously elevated by exposure to hyposmotic medium. The time course of these changes suggests that SRIF and altered osmotic pressure act on PRL secretion in at least partial independence of effects which they may have on PRL synthesis in the tilapia pituitary.

Quantitative aspects of membrane shifts in rat parathyroid cells initiated by decrease in serum calcium.

The secretory activity of parathyroid glands in rats was stimulated by decreasing the serum Ca++ concentration through constant intravenous infusion of EGTA. The morphometric analysis of the nuclear and cytoplasmic volume and of the surface area of the rough endoplasmic reticulum, Golgi complex, secretory granules and plasma membrane revealed a membrane shift from secretory granules and Golgi complex to the plasma membrane within 1 hr of calcium depression. Subsequently, between 1 and 3 hr of calcium depression, the membrane shift was from the plasma membrane to the Golgi complex. It is considered likely that these membrane shifts are related to a rise in release of parathyroid hormone by exocytosis and a subsequent increase in retrieval of plasma membrane by endocytosis--probably through the compartment of coated pits and coated and uncoated vesicles.

Actions of benzodiazepines on the neuroendocrine system

The administration of benzodiazepines to rats is associated with alterations in the secretion of anterior pituitary hormones. Although basal secretion of prolactin and thyroid stimulating hormone (TSH) was not changed by benzodiazepines, the secretory response to physiological and pharmacological stimuli was attenuated. Diazepam reduced the rise in secretion of prolactin during proestrus and the increase in release induced by stress, administration of fluoxetine plus 5-hydroxytryptophan and haloperidol. Diazepam also blocked the rise in release of TSH induced by exposure to cold. To establish the site at which benzodiazepines act, anterior pituitary binding for [ 3H]diazepam was characterized. Scatchard analysis indicated a K d of 11 nM and a B max of 27 fmol/10 6 cells. In cultures of anterior pituitary cells diazepam enhanced the inhibition of prolactin secretion produced by γ-aminobutyric acid (GABA) and dopamine. The potency of benzodiazepine analogues established that the benzodiazepine binding site in the pituitary belonged to the peripheral subtype of benzodiazepine receptors. However, the potency of analogues for inhibition of the release of prolactin and TSH following systemic administration indicates that benzodiazepines with affinity for the central subtype of receptors were the most potent. These data are interpreted to suggest that the actions of benzodiazepines on the neuroendocrine system result from their actions within the CNS on the neurons involved in the regulation of pituitary function. In addition, peripheral benzodiazepine receptors are present on cells of the anterior pituitary and these binding sites can modulate secretion of prolactin in response to its inhibitory regulators.

Temperature and Ethylene Effects on Cut Flowers of Carnation (Dianthus carophyllus L.)1

Abstract Cut carnation flowers shipped from California by air occasionally arrive at eastern markets in a senescent condition with losses greater in the warm autumn months. CO2 and C2H4 production by the flowers has a pattern similar to that of climacteric-class fruits, with senescence correlated with a rise in release of the gases. Cut carnation flowers show an enormous increase in respiratory heat with increasing temperature: 89 BTU/ton/hour at 0°C versus 14,718 at 50°C. In C2H4-free air, the flowers tolerate elevated temperatures but their vase life is reduced. Their sensitivity to C2H4 increases dramatically with increasing temperature, with the threshold concentration partially depending on prior stresses on the flowers. Flowers in containers exposed to direct sunlight developed temperatures as high as 49.5°C. Air temperatures inside containers shipped via jet aircraft were as high as 35°C. The C2H4 concentrations in the containers may reach 10.5 ppm. The remarkable resistance of cut carnation flowers to mechanical injury, combined with their low metabolic rates at low temperatures, makes refrigerated surface shipments feasible and perhaps economically desirable. Their resistance to injury seems related to their light weight, the damping action of the petals, and the lack of phenolase or readily oxidizable phenolic compounds in the petals.