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PubMed1992

Low doses of oxytocin facilitate social recognition in rats.

Social recognition of juveniles by adult male residents has been shown to be modulated by neurohypophyseal hormones. The decrease of social investigation behavior during a second encounter with the same juvenile serves as index for social recognition. In the present study it was found that low doses (0.09-6.0 ng.kg-1) of oxytocin (OXT) given subcutaneously dose dependently facilitated social recognition. The effect of OXT appeared specific, since no change in social investigation was found when a novel juvenile was tested during the second encounter. No disturbances of social recognition by the low doses of OXT could be detected, in contrast to higher doses of this hormone. Other neurohypophyseal hormones, vasopressin and vasotocin, did not facilitate social recognition when tested in the same range of low doses.

Animals↗
PubMed1978

Subclones of normal clonal prolactin cells of the rat.

We recently established a clone (2B8) of normal rat prolactin cells that secretes only prolactin into the medium. When grown in the presence of thyrotrophin-releasing hormone (TRH), estradiol (E2) or arginine vasotocin (AVT), the cells show increased production of prolactin. Subclones of single cell origin were developed from 2B8 cells exposed for 1 week to TRH, E2 or TRH plus E2. These subclones differ in their response to TRH, E2 or AVT and therefore may possess different receptors for these hormones.

Clone Cells↗
PubMed1996

ADH action on whole-cell currents by cytosolic Ca2+-dependent pathways in aldosterone-treated A6 cells.

We studied the characteristics of the basal and antidiuretic hormone (arginine vasotocin, AVT)-activated whole cell currents of an aldosterone-treated distal nephron cell line (A6) at two different cytosolic Ca2+ concentrations ([Ca2+]c, 2 and 30 nm). A6 cells were cultured on a permeable support filter for 10 approximately 14 days in media with supplemental aldosterone (1 microM). At 30 nm [Ca2+]c, basal conductances mainly consisted of Cl- conductances, which were sensitive to 5-nitro-2-(3-phenyl-propylamino)-benzoate. Reduction of [Ca2+]c to 2 nm abolished the basal Cl- conductance. AVT evoked Cl- conductances at 2 as well as 30 nm [Ca2+]c. In addition to Cl- conductances, AVT induced benzamil-insensitive nonselective cation (NSC) conductances. This action on NSC conductances was observed at 30 nm [Ca2+]c but not at 2 nm [Ca2+]c. Thus, cytosolic Ca2+ regulates NSC and Cl- conductances in a distal nephron cell line (A6) in response to AVT. Keeping [Ca2+]c at an adequate level seems likely to be an important requirement for AVT regulation of ion conductances in aldosterone-treated A6 cells.

Aldosterone↗
PubMed1998

Apical Cl- channels in A6 cells.

Short-circuit current (Isc), transepithelial conductance (Gt), electrical capacitance (CT) and the fluctuation in Isc were analyzed in polarized epithelial cells from the distal nephron of Xenopus laevis (A6 cell line). Tissues were incubated with Na+- and Cl--free solutions on the apical surface. Basolateral perfusate was NaCl-Ringer. Agents that increase cellular cAMP evoked increases in Gt, CT, Isc and generated a Lorentzian Isc-noise. The responses could be related to active, electrogenic secretion of Cl-. Arginine-vasotocin and oxytocin caused a typical peak-plateau response pattern. Stimulation with a membrane-permeant nonhydrolyzable cAMP analogue or forskolin showed stable increases in Gt with only moderate peaking of Isc. Phosphodiesterase inhibitors also stimulated Cl- secretion with peaking responses in Gt and Isc. All stimulants elicited a spontaneous Lorentzian noise, originating from the activated apical Cl- channel, with almost identical corner frequency (40-50 Hz). Repetitive challenge with the hormones led to a refractory behavior of all parameters. Activation of the cAMP route could overcome this refractoriness. All agents caused CT, a measure of apical membrane area, to increase in a manner roughly synchronous with Gt. These results suggest that activation of the cAMP-messenger route may, at least partly, involve exocytosis of a vesicular Cl- channel pool. Apical flufenamate depressed Cl- current and conductance and apparently generated blocker-noise. However, blocking kinetics extracted from noise experiments could not be reconciled with those obtained from current inhibition, suggesting the drug does not act as simple open-channel inhibitor.

Animals↗
PubMed2003

Prostaglandins modulate the renal actions of antidiuretic hormone in the Pekin duck.

The present study was designed to determine whether the responses of the avian kidney to circulating arginine vasotocin (AVT), under different osmotic conditions, involve an interaction with prostaglandins (PGs). The renal effects of intravenously infused AVT at a dose of 0.1 ng.kg(-1).min(-1) for 45 min were compared in Pekin ducks given maintenance infusions of either 200 mosmol NaCl or glucose at 1 ml.min(-1), with and without PG inhibition by indomethacin. Birds infused with glucose responded with similar degrees of AVT-induced antidiuresis with and without indomethacin, however the urinary excretion of sodium was significantly reduced when PG production was prevented. In ducks receiving saline without indomethacin, the antidiuretic response to AVT was markedly less than that in the glucose-infused birds, however, indomethacin treatment increased the degree of antidiuresis to a level similar to that in the glucose-infused ducks. The results indicate that PGs have important renotropic actions in birds and in particular modulate the antidiuretic effect of AVT in salt- and volume-loaded animals.

Animals↗
PubMed2006

Physiological and hormonal control of thermal depression in the tiger snake, Notechis scutatus.

Plasma sodium concentrations in field-caught Western tiger snakes, Notechis scutatus, from semi-arid Carnac Island (CI) varied seasonally, with snakes exhibiting significant hypernatraemia during summer and normal concentrations following autumn rain. In contrast, field-caught tiger snakes from a perennial fresh-water swamp (Herdsman Lake, HL) exhibited no significant increase in plasma sodium concentrations during summer. Laboratory-induced hypernatraemia caused thermal depression in both populations; there was a weak negative relationship between plasma sodium concentration and temperature selection that was significant for CI snakes. Hypernatraemia significantly elevated circulating concentrations of the neuropeptide arginine vasotocin (AVT) in both CI and HL snakes. CI snakes injected with a physiological dosage of AVT also evidenced thermal depression. Despite the positive correlation between AVT and both plasma sodium concentration and osmolality for laboratory snakes, field samples from CI snakes indicate that circulating levels of AVT may be influenced more by plasma osmolality than sodium levels. The data suggest that, in CI snakes, chronic dehydration in the field leads to hypernatraemia which may lead to elevated levels of AVT if plasma osmolality also increases. This will in turn invoke a depression in thermal behaviour that may improve the water economy and survival of snakes on semi-arid CI. Although HL snakes do not experience seasonal dehydration, physiological changes away from the stable homeostatic state appear to prompt the same behavioural shifts, illustrating the intrinsic nature of the thermal behaviour in different populations of the same species of snake.

Animals↗
PubMed2001

Regulation of the hypothalamic-pituitary-adrenal axis in free-living pigeons.

We studied feral free-living pigeons (Columba livia) to determine whether either unstressed or stress-induced corticosterone release was altered during a prebasic molt. The pigeons were at various stages of molt throughout the study, but corticosterone responses in molting and nonmolting birds did not differ. This was further reflected in equivalent adrenal responses to exogenous adrenocorticotropic hormone (ACTH), suggesting equivalent steroidogenic capacity of adrenal tissues during both physiological states. There was a slight change, however, in pituitary regulation during molt. Whereas exogenous arginine vasotocin (AVT) elevated corticosterone levels in nonmolting birds, during molt an equivalent dose of AVT was ineffective, suggesting that the pituitary is less sensitive to an AVT signal during molt. AVT also appears to be more effective than corticotropin-releasing factor at eliciting ACTH release in pigeons. Overall, these data indicate that pigeons regulate their corticosterone release differently during molt than other avian species studied to date.

Adrenocorticotropic Hormone↗
PubMed2000

Control of salt gland activity in the hatchling green sea turtle, Chelonia mydas.

We studied the control of salt gland secretion in hatchling Chelonia mydas. The threshold salt load to activate salt secretion was between 400 mumol NaCl 100 g bodymass (BM)-1 and 600 mumol NaCl 100 g BM-1, which caused an increase in plasma sodium concentration of 13% to 19%. Following a salt load of 2700 mumol NaCl 100 g BM-1, salt gland secretion commenced in 12 +/- 1.3 min and reached maximal secretory concentration within 2-7 min. Maximal secretory rate of a single gland averaged 415 mumol Na 100 g BM-1 h-1. Plasma sodium concentration and total osmotic concentration after salt loading were significantly higher than pretreatment values within 2 min. Adrenalin (25 micrograms kg BM-1) and the cholinergic agonist methacholine (1 mg kg BM-1) inhibited salt gland activity. Atropine (10 mg kg BM-1) reversed methacholine inhibition and stimulated salt gland secretion when administered with a subthreshold salt load. Arginine vasotocin produced a transient reduction in sodium secretion by the active gland, while atrial natriuretic factor, vasoactive intestinal peptide and neuropeptide Y had no measurable effect on any aspect of salt gland secretion. Our results demonstrated that secretion of the salt gland in C. mydas can be modified by neural and hormonal chemicals in vivo and that the cholinergic and adrenergic stimulation of an exocrine gland do not appear to have the typical, antagonist actions on the chelonian salt gland.

Animals↗
PubMed1998

Changes in pituitary and adrenal sensitivities allow the snow bunting (Plectrophenax nivalis), an Arctic-breeding song bird, to modulate corticosterone release seasonally.

Several free-living avian species have recently been shown to seasonally modulate corticosterone release in response to capture and restraint. We examined possible mechanisms underlying seasonal adrenocortical modulation in snow buntings (Plectrophenax nivalis), a species that breeds and molts (the energetically costly replacement of feathers) in the Alaskan Arctic Snow buntings dramatically reduced baseline and maximal corticosterone titers during molt compared to the breeding season. This effect is not explained by changes in either corticosterone binding protein capacity or the overall condition of the bird (assessed by weight and fat storage). Although the adrenal's capacity to secrete corticosterone is reduced during molt, adrenal insensitivity does not fully explain reduced maximal output since exogenous adrenocorticotropic-hormone enhanced corticosterone release during both seasons. In contrast, no exogenous adrenocorticotropic hormone releasing factor (corticotrophin-releasing factor, arginine vasotocin or mesotocin) enhanced corticosterone secretion during molt. This suggests that the pituitary's endogenous adrenocorticotropic secretion was maximal in response to capture and handling, making the pituitary an important site regulating corticosterone levels. Taken together, these results indicate that seasonal modulation of corticosterone release in this species is controlled at both the adrenal and pituitary glands.

Adrenal Glands↗
PubMed2002

Regulation of urea permeability in frog urinary bladder by prostaglandin E(2).

The present study was performed to investigate the role of prostaglandin E(2) (PGE(2)) in the regulation of urea transport in the frog urinary bladder, which is known to occur via a specialized arginine-vasotocin- (AVT-) regulated urea transporter. The bladders isolated from Rana temporaria L. were filled with amphibian Ringer solution containing 370 Bq/ml (0.01 microCi/ml) of [14C]urea, and urea permeability ( P(urea)) was determined by sampling the serosal and mucosal bathing medium at 30-min intervals for measurement of radioactivity. It was found that, from the serosal side, PGE(2) (10 nM to 1 microM) caused a dose-dependent increase in P(urea) [(7.2+/-1.8)x10(-6) cm/s in the presence of 0.5 microM PGE(2)versus (1.0+/-0.2)x10(-6) cm/s in control, n=9, P<0.001]. As in response to AVT, the PGE(2)-induced P(urea)reached a maximum in 1-1.5 h after the agonist was added. The stimulatory effects of PGE(2) and AVT applied together were not additive. PGE(2)-induced urea transport was strongly inhibited by nearly 75% in the presence of mucosal or serosal phloretin (10(-4) M). P(urea) was enhanced up to (4.7+/-0.8)x10(-6) cm/s (n=12, P<0.001) by butaprost (5 x 10(-6) M), a selective EP(2) receptor agonist, while sulprostone (EP(1)/EP(3) agonist, 10(-6) M) caused no changes in P(urea). PGE(2)dose-dependently increased the content of cAMP in mucosal epithelial cells (control: 18.0+/-1.8; 10(-6) M PGE(2): 74.2+/-9.3 pmol cAMP/mg protein per 30 min, n=7, P<0.001). Phorbol esters did not alter PGE(2)-induced P(urea), whereas H-89 (20 microM), a protein kinase A inhibitor, reduced it by 45.1+/-9.9% ( n=5, P<0.05). PGE(2)did not change the AVT-stimulated P(urea) measured in isoosmotic conditions, but inhibited the last one in the presence of a serosa-to-mucosa osmotic gradient. The data obtained show that, in the frog urinary bladder, PGE(2)is a stimulator of phloretin-inhibitable urea transport. Its effect seems to be mediated by EP(2) receptor-coupled generation of intracellular cAMP.

Algorithms↗
PubMed2003

Differential distribution of melatonin receptors in the pituitary gland of Xenopus laevis.

A major target site for melatonin action is thought to be the pituitary gland. We have detected differential expression and co-localization of the Mel(1a) and Mel(1c) receptors in cells of the Xenopus laevis pituitary gland. Sections of Xenopus pituitary glands were labeled with Mel(1a) and/or Mel(1c) antibodies, in combination with antibodies to arginine vasotocin (AVT), alpha-melanocyte stimulating hormone (alpha-MSH), prolactin (PRL), and luteinizing hormone (LH). Mel(1a) immunoreactivity was localized to cells of the pars intermedia and to elements within the pars nervosa. Mel(1c) immunoreactivity was also localized to the pars nervosa, and significant labeling was also observed in discrete clusters of cells in the pars distalis. Mel(1a) was absent from the pars distalis, while Mel(1c) was absent from the pars intermedia. Mel(1a) and Mel(1c) were co-localized in the pars nervosa. AVT was present in the pars nervosa, and appeared to be localized to the cell clusters of the pars distalis in which the Mel(1c) receptor was localized. alpha-MSH co-localized with the Mel(1a) receptor in the pars intermedia. LH appeared to localize to many of the cells in the pars distalis, with the notable exception of the Mel(1c) receptor-positive clusters of cells. PRL did not appear to co-localize with either melatonin receptor. The pattern of differential expression of the Mel(1a) and Mel(1c) receptors suggests that the receptors specifically mediate the cellular response to melatonin binding in the specific cell populations.

Animals↗
PubMed1996

Distribution of AVT gene expressing neurons in the prosencephalon of japanese quail and chicken.

Detailed anatomical studies about the distribution of arginine-vasotocin (AVT) gene expressing neurons in the avian brain are so far non-existent. Most of the investigations are limited to discrete brain nuclei in the chicken and concern particular experimental conditions. Since no data on AVT gene expression are up to now available in Japanese quail, we report here the distribution of AVT mRNA containing neurons within the prosencephalon of this bird and a comparison with the same system of the chicken. The AVT mRNA containing perikarya were detected with a specific AVT cDNA probe directed toward the distal 3' glycopeptide encoding part of the chicken AVT gene. The specificity of the probe was tested by Northern and Southern blot analysis. The AVT gene expressing neurons showed the same pattern of distribution in both species; however, a larger number of labelled neurons was observed in the chicken by visual inspection of the sections. AVT gene expressing neurons were distributed within the hypothalamus (in the medial and ventral aspects of the rostral preoptic area, in the lateral forebrain bundle, close to the ependyma of the third ventricle and in several periventricular hypothalamic nuclei) and in some extrahypothalamic regions (around the nucleus rotundus, close to the nucleus commissurae pallii and in a region probably corresponding to the nucleus strial terminalis). AVT gene expressing neurons were observed close to the organum septi laterale of the chicken. Taken together, these results confirm the specificity of the employed probe and its suitability for further studies on the modulation of AVT gene expression in quail.

Animals↗
PubMed1989

Vasopressin receptors in human pregnant myometrium and decidua: interactions with oxytocin and vasopressin agonists and antagonists.

Saturation analysis and competition experiments were performed to identify and characterize [3H]arginine vasopressin binding to human myometrium and decidua in late pregnancy. [3H]Arginine vasopressin bound with affinity similar to that of [3H]oxytocin to both tissues (dissociation constant 1 to 2 nmol/L). The concentration of [3H]arginine vasopressin binding sites was high, particularly in decidua, but in all instances was about 50% to 60% of [3H]oxytocin binding. Analogs with selective oxytocic potency (4-threonine oxytocin, isotocin) had high affinity to both [3H]arginine vasopressin and [3H]oxytocin binding sites, as did analogs with both oxytocic and vasopressor activity (vasotocin). Analogs with selective antidiuretic activity (1-deamino-8-D-arginine vasopressin) showed drastically reduced affinity to [3H]oxytocin binding sites and relatively low but significantly higher affinity to [3H]arginine vasopressin binding sites. A new oxytocin antagonist (RW22164 or [1-deamino-2D-tyrosine-(O-ethyl)-4-threonine-8-ornithine]oxytocin) competitively bound to both binding sites. Its affinity to [3H]oxytocin binding sites was greater than to [3H]arginine vasopressin binding sites whereas the relative affinities of a predominantly vasopressor antagonist [Manning compound) were reversed, suggesting the presence of distinct receptors for oxytocin and arginine vasopressin in pregnant human myometrium and decidua.

Animals↗
PubMed1985

The action of centrally administered arginine vasopressin on blood pressure in the conscious rabbit.

In addition to its peripheral endocrine actions, arginine vasopressin (AVP) has been implicated in the central control of blood pressure. Intracerebroventricular (i.c.v.) injections (0.01-1.0 nmol) of AVP or arginine vasotocin (AVT), but not oxytocin (OXY), into unanesthetized rabbits caused a rapid, dose related rise in blood pressure as well as increases in heart rate. The lowest centrally administered dose of AVP and AVT (0.01 nmol) had no effect on blood pressure when given intravenously. In search of tissue locus for the pressor effect of AVP microinjection of AVP and OXY into the posterior hypothalamus and septum of conscious rabbits was without effect. However, microinjection (0.01-0.04 nmol) of AVP into the nucleus tractus solitarius of anesthetized rabbits caused a rise in blood pressure similar to the response seen after i.c.v. injection. Comparable volumes of the vehicle into the ventricle or the tissue sites had no effect on resting blood pressure. The pressor response after AVP given i.c.v. was significantly reduced up to 3 h after administration of the ganglionic blocker, chlorisondamine HCl. The central antagonist, d(CH2)5Tyr (Me) vasopressin, eliminated the usual increase in blood pressure after administration of AVP in half the animals tested. The results indicate that AVP acts centrally to mediate cardiovascular responses in unanesthetized as well as anesthetized rabbits.

Animals↗
PubMed1987

Somatostatin and calcitonin stimulate neurite regeneration of molluscan neurons in vitro.

Isolated neurons from the gastropod Physella heterostropha fail to regenerate their neurites if cultured in defined medium in the absence of growth factors. A significant number of cultured neurons extend neurites if they are cultured in brain-conditioned or hemocyte-conditioned medium. Synthetic somatostatin and salmon calcitonin also stimulate neurite regeneration in a dose-dependent manner. Thyrotropin-releasing hormone, arginine vasotocin, and eledoisin fail to promote neurite outgrowth. It is concluded that, like other molluscan neurons, isolated neurons from Physella require the presence of factors that are released by brain tissue or are present in the hemolymph, and that somatostatin and calcitonin can, in part, substitute for the endogenous neurite-regenerating activities.

Animals↗
PubMed1994

Vasotocinergic innervation of sexually dimorphic medial preoptic nucleus of the male Japanese quail: influence of testosterone.

The distribution of vasotocin (VT)-immunoreactive (IR) fibers was described in the preoptic and septal regions of the male quail brain. The density of VT-IR fibers was measured in the sexually dimorphic preoptic nucleus (POM) and lateral septum (SL) of adult male quail (Coturnix japonica) by means of quantitative image analysis. Experimental manipulations of the hormonal environment in the peripubertal period influenced this distribution. In both regions, the VT immunoreactivity was reduced or absent when males were castrated. The immunoreactivity was restored to its original level in castrated males by Silastic implants of testosterone. These changes were anatomically specific as evidenced by the fact that the density of VT fibers did not vary in the hypothalamo-neurohypohysial tract as a function of the endocrine condition of the subjects. No change was also observed in the number of VT-IR cells in the periventricular region close to the POM. Previously published data show that VT or its mammalian homolog, vasopressin are implicated in the control of a wide range of instinctive behaviors. The steroid-dependent VT afferents to the POM, a key area controlling male copulatory behavior in quail could therefore be involved in the control of the sexual behavior in this species. The outputs of the POM which contains steroid-receptors could therefore be modulated by steroids in two different ways: directly through the steroid receptors it contains and indirectly through its steroid-sensitive peptidergic afferents.

Animals↗
PubMed1994

Vasopressin-induced calcium signaling in cultured hippocampal neurons.

We recently demonstrated that the neural peptide vasopressin (AVP) can act as a neurotrophic factor for hippocampal nerve cells in culture. Because the neurotrophic effect of vasopressin is mediated by the V1 receptor, we investigated AVP activation of calcium signaling pathways in cultured hippocampal neurons. Results of this investigation demonstrate that exposure of cultured hippocampal neurons prelabeled with [3H]myo-inositol to vasopressin induced a significant accumulation of [3H]inositol-1-phosphate ([3H]IP1). The selective V1 vasopressin receptor agonist, [Phe2, Orn2]vasotocin, induced a significant accumulation of [3H]IP1 whereas a selective V2 vasopressin receptor agonist, [deamino1, D-Arg8]-vasopressin, did not. Moreover, V1 agonist-induced accumulation of [3H]IP1 was blocked by the selective V1 vasopressin receptor antagonist d(CH2)5[Tyr(Me)2]-vasopressin. V1 agonist-induced accumulation of [3H]IP1 was concentration dependent and exhibited a steep inverted U-shaped curve that included both stimulation and inhibition of [3H]IP1 accumulation. Time course analysis of V1 agonist-induced accumulation of [3H]IP1 revealed significant increase by 20 min which continued to be significantly elevated for 60 min. Investigation of the effect of closely related peptides on [3H]IP1 accumulation indicated that the vasopressin metabolite peptide AVP4-9 and oxytocin significantly increased [3H]IP1 accumulation whereas the vasopressin metabolite peptide AVP4-8 did not. AVP4-9 and oxytocin induced [3H]IP1 accumulation were blocked by the V1 vasopressin receptor antagonist d(CH2)5[Tyr(Me)2]-vasopressin. V1 receptor activation was associated with a pronounced rise in intracellular calcium. Results of calcium fluorometry studies indicated that V1 agonist exposure induced a marked and sustained rise in intracellular calcium that exhibited oscillations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗