Biomedical subjects

O M Youngren

Publications and source records attributed to O M Youngren.

At least 19 recordsLinked to original sources

PubMed2006

Identification of dopamine, gonadotrophin-releasing hormone-I, and vasoactive intestinal peptide neurones activated by electrical stimulation to the medial preoptic area of the turkey hypothalamus: a potential reproductive neuroendocrine circuit.

The neural and neurochemical substrates regulating reproduction in birds remain vaguely defined. The findings that electrical stimulation in the medial preoptic area (ES/MPOA) or intracerebroventricular infusion of dopamine (DA) stimulated luteinising hormone (LH) and prolactin (PRL) release in female turkeys, led to the suggestion that ES/MPOA might help to clarify the DA circuitry regulating LH and PRL. We used c-fos mRNA and tyrosine hydroxylase immunoreactivity as measured by double in situ hybridisation/immunocytochemistry (ISH/ICC) to determine which group/subgroup of DA neurones was activated following unilateral ES/MPOA. To establish that the reproductive neuroendocrine system was activated, double ISH/ICC was also conducted on c-fos/gonadotrophin-releasing hormone-I (GnRH-I) and c-fos/vasoactive intestinal peptide (VIP). Changes in circulating LH and PRL were determined by radioimmunoassay. Unilateral ES/MPOA (100 microA, right side) of anaesthetised laying turkeys for 30 min increased circulating LH and PRL levels. It also induced c-fos mRNA expression on the ipsilateral side by all GnRH-I neurones within the septopreoptic region, implying that GnRH-I neurones in this region share similar circuitry. VIP neurones within the nucleus infundibularis were the only VIP group to show c-fos mRNA expression, suggesting their involvement in ES/MPOA induced PRL release. c-fos mRNA expression was also observed in a subgroup of DA neurones in the nucleus mamillaris lateralis (ML). To our knowledge, the present study is the first to show that activation of DAergic cells in the ML is associated with the activation of GnRH-I and VIP neurones and the release of LH and PRL. It is likely that ES/MPOA activated VIP/GnRH-I neurones via activation of DA neurones in the ML, as this was the only DA subgroup that showed c-fos mRNA expression.

Analysis of Variance↗

PubMed1999

An opioid pathway in the hypothalamus of the turkey that stimulates prolactin secretion.

Circulating prolactin (PRL) levels increase when dynorphin is infused into the turkey brain. This study tested the hypothesis that centrally infused dynorphin requires an intact vasoactive intestinal peptide (VIP) system in order to stimulate turkey PRL secretion. It also investigated the roles of the dopaminergic and serotonergic systems in dynorphin-induced PRL release. Drugs were infused into the third ventricle of anesthetized laying turkeys via stereotaxically guided cannulae and circulating blood was assayed for changes in PRL levels. When a highly selective kappa opioid receptor antagonist was given prior to dynorphin injection, the PRL response to dynorphin was almost totally blocked. The coinfusion of either a serotonin (5-HT) or a D(1) dopamine (DA) receptor antagonist with dynorphin prevented the increase in PRL observed in birds when dynorphin was infused alone. On the other hand, the kappa opioid receptor antagonist failed to prevent the 5-HT-induced release of PRL. In hens actively immunized against VIP, infused dynorphin was unable to increase plasma PRL levels and infused VIP gave a muted PRL rise, while large increases in PRL were seen in nonimmunized birds receiving the same infusions. These data show that: (1) dynorphin stimulates PRL secretion by activating kappa opioid receptors in the avian hypothalamus, and (2) dynorphin, 5-HT, DA, and VIP stimulate avian PRL secretion via a common pathway expressing kappa opioid, serotonergic, dopaminergic, and VIPergic receptors at synapses arranged serially in that functional order, with the VIPergic system as the final mediator (releasing factor).

Animals↗

PubMed1998

Serotonergic stimulation of avian prolactin secretion requires an intact dopaminergic system.

In order to ascertain if prolactin (PRL) secretion stimulated by serotonin (5-HT) was mediated by the dopaminergic system, both dopamine (DA) and 5-HT were infused into the third ventricle of anesthetized laying turkeys in conjunction with the D1 DA receptor antagonist R(+)-SCH-23390 HCl or the 5-HT receptor antagonist Mianserin HCl. When infused alone at the rate of 10 nmol/min, both DA and 5-HT increased circulating PRL levels significantly (P < 0. 05) after 20 min (111.0 +/- 19.0 to 334.0 +/- 115.1 ng/ml and 93.3 +/- 13.2 to 173.8 +/- 33.3 ng/ml, respectively). When infused in conjunction with the D1 DA antagonist, the stimulatory effect of both DA and 5-HT on PRL release was significantly suppressed. The 5-HT antagonist completely blocked 5-HT-stimulated PRL release when infused at the rate of 10 nmol/min. When the 5-HT antagonist was co-infused with DA, PRL levels significantly increased (33.5 +/- 3.3 to 112.2 +/- 19.7 ng/ml) after 30 min, an increase that did not differ significantly from that caused by DA alone (63.2 +/- 16.4 to 144.5 +/- 44.1 ng/ml). These data suggest that 5-HT stimulation of PRL secretion requires an intact dopaminergic system and that 5-HT synapses are located further upstream than DA synapses along the PRL-releasing pathway within the avian hypothalamus.

Animals↗

PubMed1998

Vasoactive intestinal peptide secretion by turkey hypothalamic explants.

The objective of this study was to culture turkey hypothalami and examine vasoactive intestinal peptide (VIP) release during the turkey reproductive cycle. The release of VIP was studied employing a computer-guided perifusion system. Hypothalami were perifused with Krebs-Ringer bicarbonate medium for 10 or 15 h at a flow rate of 40 microliter/min, and perifusate was collected at 5-min intervals. Basal VIP secretion increased (p < 0.05) over time, and no differences in release rate were noted between reproductive stages. Basal VIP release during perifusion was episodic throughout each experimental period. Perifusion with dopamine (DA; 10 and 100 nmol/min) in incubating hens stimulated VIP release in a dose-dependent manner. There were no significant differences (p > 0.05) in VIP release in response to DA stimulation between hypothalamic fragments obtained from nonphotostimulated and incubating birds. The data suggest that 1) a VIP pulse generator appears to be located within the turkey hypothalamus, on the basis of the observed pulsatile release of VIP; 2) hypothalamic secretion of VIP is augmented by removal of inhibitory factors residing outside of the hypothalamus, or by the loss of negative feedback mechanisms that inhibit VIP release; and 3) mechanisms responsible for altering VIP release during different reproductive conditions may lie external to the hypothalamus.

Animals↗

PubMed1998

Regulation of prolactin secretion by dopamine and vasoactive intestinal peptide at the level of the pituitary in the turkey.

This study investigated the capability of dopamine (DA) to prevent avian prolactin (PRL) secretion by antagonizing the PRL-releasing factor, vasoactive intestinal peptide (VIP), at the level of the pituitary. To test this hypothesis, combined intracranial and intrapituitary infusions of DA, DA agonists, and VIP, plus electrical stimulation of the medial preoptic area (ES/POM), were used to characterize the actions of DA on PRL secretion in anesthetized laying turkey hens. Infused into the third ventricle at the rate of 10 nmol/min, DA induced a 2.8-fold increase in circulating PRL levels (63.8 +/- 15.1 to 181.3 +/- 44.3 ng/ml, p < 0. 05), similar to the 3.1-fold PRL increase induced by ES/POM (65 +/- 10.3 to 199.1 +/- 57.3 ng/ml, p < 0.05). Infused into the anterior pituitary at the rate of 15 ng/min, VIP induced a 2.2-fold increase in PRL (78.6 +/- 22.9 to 173.6 +/- 39.5 ng/ml, p < 0.05). When DA (10 nmol/min) was infused into the anterior pituitary it completely blocked both ES/POM- and VIP-induced PRL secretion. The D2 DA receptor agonist R- (-) -Propylnorapomorphine HCl inhibited VIP-induced PRL secretion at the level of the anterior pituitary, allowing only an insignificant rise in PRL (54.8 +/- 14.3 to 73.9 +/- 21.6 ng/ml, p > 0.05), while the D1 DA receptor agonist (+/-)-SKF-38393 HCl failed to prevent VIP-induced PRL release, allowing PRL to rise 2.5-fold (49.1 +/- 10.8 to 121.0 +/- 34.8 ng/ml, p < 0.05). Pituitary infusion of DA, DA agonists or vehicle alone caused no change in PRL levels. The data showed that DA prevented avian PRL secretion by blocking the action of VIP at the level of the anterior pituitary. DA effected this blockade of PRL via D2 DA receptors residing within the anterior pituitary. The data also suggested that there were no stimulatory D1 DA receptors related to PRL secretion in the avian anterior pituitary.

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PubMed1998

Transcriptional changes in hypothalamic vasoactive intestinal peptide during a photo-induced reproductive cycle in the turkey.

To characterize further vasoactive intestinal peptide (VIP) as the prolactin-releasing factor in avian species, the present study examined hypothalamic VIP transcription and plasma prolactin (PRL) levels during the turkey reproductive cycle. The contribution of transcription to hypothalamic VIP mRNA steady-state levels and VIP content in response to gonadal stimulating photoperiod was also investigated. Nuclear run-on transcription assays were performed using nuclei isolated from hypothalami. Cytoplasmic VIP mRNA levels, and VIP content in the median eminence and plasma PRL levels were determined by Northern blot analysis and radioimmunoassays respectively. The alterations in VIP transcription mirrored the changes in cytoplasmic VIP mRNA and VIP content during the reproductive stages. VIP transcription, cytoplasmic VIP mRNA level and VIP content were lowest in non-photostimulated birds, higher (P<0.05) in laying hens, and greatest (P<0.05) in incubating birds. These increases paralleled the changes in circulating plasma PRL levels. Changes in VIP transcription (P>0.05) were not observed during the transition from incubation to photorefractoriness, even though there was a sharp decline in circulating plasma PRL levels (P<0.05). Following photostimulation, VIP transcription, cytoplasmic VIP mRNA levels, and VIP content increased as the hens progressed towards sexual maturity (P<0.05), and these increases were correlated with an increased plasma PRL level. These results suggest that VIP is regulated in large part at the transcriptional level during the turkey reproductive cycle and that this transcriptional regulation is coupled to the photo-induced increase in PRL secretion.

Animals↗

PubMed1997

Dopamine receptors influence vasoactive intestinal peptide release from turkey hypothalamic explants.

Vasoactive intestinal peptide (VIP) is a significant prolactin-releasing factor (PRF) in avian species, and dopamine (DA) exhibits both a stimulatory and inhibitory influence upon this prolactin (PRL) secretion. The stimulatory effect of DA upon PRL release appears to be mediated by VIP. This study investigated DAergic actions upon VIP release using turkey hypothalamic explants perifused with DA and its agonists or antagonists. VIP release was stimulated by DA in a dose-dependent manner (10 nmol DA/min, from 67.2 +/- 3.9 to 164.3 +/- 3.1 pg/5 min; 100 nmol DA/min, from 70.1 +/- 3.2 to 291.0 +/- 7.5 pg/5 min; 1,000 nmol DA/min, from 72.0 +/- 4.8 to 501.0 +/- 24.7 pg/5 min). The D1 DA receptor antagonist (R+)-SCH-23390 HCl completely negated the stimulatory effect of DA (100 nmol/min) upon VIP release. Perifusion with the D2 DA receptor antagonist S(-)-eticlopride HCl by itself stimulated VIP release from the hypothalamic explants, increasing VIP from 38.1 +/- 5.3 to 161.9 +/- 9.7 pg/5 min, where release stabilized until perifusion was terminated. The D1 DA agonist (+)-SKF-38393 HCl increased VIP release from 52.7 +/- 4.6 to 192.6 +/- 16.9 pg/5 min, and this stimulated release was partially inhibited by the D2 DA receptor agonist R(-)-NPA HCl (from 192.6 +/- 16.9 to 139.7 +/- 13.8 pg/5 min). These results suggest that VIP secretion is in part regulated by possible opposite actions between stimulatory D1 and inhibitory D2 DA receptors in the turkey hypothalamus.

Animals↗

PubMed1996

Dopaminergic control of prolactin secretion in the turkey.

The stimulatory and inhibitory effects of dopamine (DA) upon avian prolactin (PRL) secretion suggest that, in birds, these actions are mediated by multiple DA receptors. To test this hypothesis, combined intracranial infusions of DA and selective D1 or D2 DA receptor blockers, plus electrical stimulation (ES) of the brain and vasoactive intestinal peptide (VIP) immunoneutralization, were used to characterize the actions of DA on PRL secretion in the turkey. Blockade of D1 DA receptors prevented the increase in circulating PRL observed in response to infusion of stimulatory concentrations of DA or to ES. Stimulatory infusions of DA also failed to increase circulating PRL in birds immunized against VIP. Results from infusion of the D2 DA receptor antagonist were unclear. Low concentrations had no effect, while the highest concentration (100 nmol/min) produced an increase in plasma PRL. At the high concentration the drug may be affecting PRL secretion by (1) acting nonspecifically, (2) acting as a partial DA agonist on D1 DA receptors, or (3) diffusion to the pituitary and blockade of D2 receptors there. These data suggest that avian PRL secretion is mediated by D1 DA receptors within the brain and that the stimulatory effect of DA upon PRL secretion requires an intact VIPergic system.

Animals↗

PubMed1996

Photoperiod mediates the ability of serotonin to release prolactin in the turkey.

Photostimulation (PS) of turkeys increases the number of hypothalamic vasoactive intestinal peptide (VIP)-immunoreactive neurons, the number of anterior pituitary VIP binding sites, and prolactin (PRL) secretion. Serotonin (5-HT) was recently shown to stimulate PRL secretion through VIP. This study tested the hypothesis that 5-HT's ability to induce PRL secretion is mediated by reproductive status and/or photoperiod in normally cycling turkey hens. Initially, saline or 5-HT was infused into the third ventricle of nest-deprived, previously incubating (ND) hens for 60 min at rates of 0.1, 1.0, or 10 nmol/min. The results led to use of the 10 nmol/min infusion rate for the remaining 5-HT infusions. Next, 5-HT was infused into short-day (SD;6), laying (6), ND (5), and photorefractory (P/R;6) hens. Plasma PRL was elevated in all groups except for the SD hens (P < 0.05). In Experiment 3, VIP was infused into the median eminence of SD (6), laying (5), and P/R (5) hens, increasing circulating PRL levels in all three groups (P < 0.05). Finally, SD hens were photostimulated for 0, 3, or 10 days and then infused with 5-HT. Only the birds which were photostimulated for 10 days exhibited elevated plasma PRL (P < 0.05). In conclusion, PS regulates PRL secretion at the hypothalamic level and more than 3 days of PS are required for 5-HT-ergic stimulation of PRL secretion.

Animals↗

PubMed1996

Effect of maternal passive immunization against vasoactive intestinal peptide on prolactin secretion in turkey poults.

The purpose of this study was to examine the role of vasoactive intestinal peptide (VIP) in prolactin (PRL) release in young turkey poults. Poults obtained from hens immunized with keyhole limpet hemocyanin (KLH)-chicken VIP (cVIP-KLH) conjugate or with KLH alone were used in this study. Plasma VIP antibody was tested by means of monoiodinated cVIP. Plasma samples were prediluted (1:100) in 0.05 EDTA PBS and used as a source of primary antibody in a cVIP-binding assay. Antibody levels averaged 50.8 +/- 10.3% at hatch and then declined with age to a level of 5.0 +/- 2.1% after 3 wk. Plasma PRL concentration was lower in cVIP-KLH-immunized poults (p < 0.05) than in KLH-immunized birds. Exogenous VIP administration at 7 days of age (7.8 micrograms/kg) increased plasma PRL level (p < 0.05) to a peak value of 359 +/- 32 ng/ml in the KLH-immunized birds. A smaller increase (p < 0.05) was obtained when the KLH-immunized poults received injections at 2 and 3 wk of age. The PRL response to cVIP administration was not observed in 1- and 2-wk-old poults maternally immunized with cVIP-KLH. Similarly, electrical stimulation of the ventromedial nucleus of the hypothalamus, at 1 and 8 days of age, induced a significant increase in the plasma PRL level of maternally KLH-immunized birds but not in maternally cVIP-KLH-immunized birds. These findings suggest that cVIP is a PRL-releasing factor in young turkey poults, similar to the finding in adult turkey hens.

Animals↗

PubMed1995

The stimulatory and inhibitory effects of dopamine on prolactin secretion in the turkey.

Dopamine (DA) was infused into the third ventricle of anesthetized laying turkey hens at various concentrations to determine its effect on both basal prolactin (PRL) levels and ongoing electrically induced PRL secretion. The infusion of DA at rates of 1.0 or 10.0 nmol/min resulted in dose dependent increases in plasma PRL. These infusions had no inhibitory effect on electrically stimulated PRL release. The infusion of DA at 100.0 or 500.0 nmol/min caused no stimulation of PRL secretion and totally inhibited the PRL response elicited by electrical stimulation of the medial preoptic nucleus. These results show that dopaminergic influences are involved in both stimulating and inhibiting avian PRL secretion and suggest possible biphasic actions of DA within the brain.

Animals↗

PubMed1995

Serotonergic stimulation of prolactin secretion is inhibited by vasoactive intestinal peptide immunoneutralization in the turkey.

The neuronal mechanisms that govern prolactin (PRL) secretion in the turkey appear to involve monoaminergic systems. Considerable evidence indicates that serotonin (5-HT), acting centrally, is a potent stimulator of PRL secretion. This study, using birds actively immunized against VIP, tests the hypothesis that 5-HT stimulates PRL secretion by releasing vasoactive intestinal peptide (VIP). Nonimmunized turkeys were injected ip with saline, quipazine (5-HT agonist; 5 mg/kg), methysergide (5-HT antagonist; 8 mg/kg), or methysergide plus quipazine, and VIP-immunized birds were injected with saline or quipazine. Quipazine increased plasma PRL levels from 26.8 +/- 7.1 ng/ml at Time 0 to a peak value of 148.1 +/- 31.4 ng/ml 2 hr after infection. Pretreatment with methysergide or VIP-immunoneutralization abolished the PRL response to quipazine. Intraventricular infusion of 5-HT (1 nmol/min) caused plasma PRL to rise from a baseline of 16.3 +/- 2.6 ng/ml to 85.2 +/- 14.3 ng/ml after 30 min in nonimmunized control birds. Serotonin infusion did not induce PRL secretion in the VIP-immunized birds. These findings suggest that serotonergic stimulation of PRL secretion in the female turkey requires a functional VIPergic system.

Animals↗

PubMed1994

Active immunization with vasoactive intestinal peptide prevents the secretion of prolactin induced by electrical stimulation of the turkey hypothalamus.

Immunoneutralization of endogenous vasoactive intestinal peptide (VIP) by active immunization with chicken VIP (cVIP) reduced both basal circulating prolactin (PRL) and steady-state levels of pituitary PRL mRNA in the turkey. This immunoneutralization severely curtailed the plasma PRL response induced by infusion of cVIP into the median eminence, and totally blocked the plasma PRL release effected by electrical stimulation of the medial preoptic nucleus. This is the first demonstration that a stimulated PRL secretion can be blocked by neutralizing VIP availability. These findings imply that among the neurochemicals released by electrical stimulation, only VIP directly stimulates PRL secretion. In addition to serving as a PRL releasing factor, VIP also appears to be involved in the regulation of pituitary PRL mRNA expression.

Animals↗

PubMed1994

Role of vasoactive intestinal peptide in the control of prolactin-induced turkey incubation behavior. I. Acute infusion of vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) secretion. Ovine PRL induces incubation behavior in avian species. This study was designed to determine whether VIP can elevate plasma PRL for up to 3 h. Saline or porcine VIP (pVIP; 30, 60, or 150 ng/min) was infused into the median eminence of laying turkeys for 1 h. The 60- and 150-ng doses of pVIP increased plasma PRL (p < 0.01), whereas the 30-ng dose was insignificant. Pituitary PRL content decreased in pVIP-treated turkeys. Two-hour infusion of 60 or 150 ng chicken VIP (cVIP)/min produced similar elevations of plasma PRL (p < 0.001), which declined within 80 min. Both treatments induced insignificant increases in pituitary PRL mRNA. Saline or cVIP (30, 60, or 60 [pulsed] ng/min) was infused into the median eminence for 3 h. Sixty ng cVIP/min induced the largest PRL release (p < 0.05). The pulsatile and low-cVIP treatments resulted in release of a significant amount of PRL in comparison to the saline treatment (p < 0.01). All cVIP treatments resulted in decreased pituitary PRL content (p < 0.05). The 60-ng dose increased PRL mRNA (p < 0.1). This study shows that 60 ng VIP/min causes the maximum PRL release in laying turkeys. However, pituitary PRL content is depleted and PRL synthesis cannot maintain PRL secretion at high levels.

Animals↗

PubMed1994

Role of vasoactive intestinal peptide in the control of prolactin-induced turkey incubation behavior. II. Chronic infusion of vasoactive intestinal peptide.

Hyperprolactinemia is associated with incubation behavior in avian species. Increased nesting activity is a major indication of incubation behavior. Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) secretion from the anterior pituitary. The goal of this study was to induce incubation behavior by stimulating PRL through chronically infusing VIP into the third ventricle of turkey brains. In experiment 1, porcine VIP (pVIP) was infused into the median eminence at a rate of 60 ng/min for 7 days by means of osmotic pumps implanted s.c.. Plasma PRL increased significantly in the pVIP-treated turkeys (p < 0.001). Although egg laying was not affected by the pVIP infusion, the mean oviduct weight decreased (p < 0.057). In experiment 2, saline or pVIP (30 or 60 ng/min) was infused into the third ventricle of laying turkeys for 12 days. Both pVIP treatments increased plasma PRL for 9 days (p < 0.05). The 30-ng pVIP/min infusion decreased nesting activity, plasma LH, ovary and oviduct weight, hypothalamic GnRH I, and anterior pituitary VIP receptors (p < 0.1). However, ovine PRL infusion (20.8 ng/min) into the same turkey flock increased nesting activity (p < 0.01). In conclusion, pVIP does not induce incubation behavior in laying turkeys.

Animals↗

PubMed1993

Immunohistochemical localization of chicken gonadotropin-releasing hormones I and II (cGnRH I and II) in turkey hen brain.

The distribution of cells and fibers immunoreactive (ir) for either chicken gonadotropin-releasing hormone I (cGnRH I; [Gln8]GnRH) or II ([His5,Trp7,Tyr8]GnRH) was determined in brains of turkey hens to reveal whether these peptides occur in separate neuronal systems. ir-cGnRH I cells were located: along the medial aspect of the ventriculus lateralis, nucleus accumbens, and bed nucleus of the stria terminalis; ventral to the tractus septomesencephalicus and extending medially to the third ventricle, and caudally into the lateral hypothalamic area; and in a diffuse band extending from the nucleus preopticus medialis to the nucleus dorsomedialis anterior thalami. cGnRH I fibers were evident in these areas in addition to the hippocampus, nucleus subhabenularis medialis, nucleus ventromedialis hypothalami, and median eminence. Two groups of ir-cGnRH II cells were observed: a magnocellular group lying between the substantia grisea centralis and the nucleus ruber; and a parvicellular group lying medial to the nucleus of the basal optic root and extending into the lateral hypothalamic area. ir-cGnRH II fibers were prominent in limbic structures (cortex piriformis, lateral to nucleus taeniae, hippocampus); olfactory areas (tuberculum olfactorium, nucleus subhabenularis lateralis, nucleus septalis lateralis); areas that in other avian species have steroid-concentrating cells or receptors (medial edge of lobus parolfactorius, nucleus septalis medialis, nucleus periventricularis magnocellularis, nucleus dorsomedialis posterior thalami); and areas containing ir-GnRH I cells or fibers but not in median eminence. These results suggest that cGnRH I and II occur in separate neuronal systems and that cGnRH II does not directly promote pituitary gonadotropin secretion.

Animals↗

PubMed1993

Effect of reproductive condition on luteinizing hormone and prolactin release induced by electrical stimulation of the turkey hypothalamus.

In the turkey, the onset of incubation behavior is associated with decreased luteinizing hormone (LH) and increased prolactin (PRL). This study was designed to clarify the contribution of the hypothalamus and the anterior pituitary to the changes in plasma LH during the reproductive cycle of the turkey. Plasma LH and PRL were measured in anesthetized turkey before, during, and after electrical stimulation in the median eminence. In one experiment, luteinizing hormone releasing hormone (LHRH; 4 micrograms/kg) was injected intramuscularly 30 min after termination of electrical stimulation, and blood samples were obtained 5, 10, 20, and 30 min after injection. Electrical stimulation in the median eminence significantly increased (P < 0.05) plasma LH of laying (LAY), nest-deprived, previously incubating (NEST DEP), and photorefractory (REFRAC) hens, but not of photosensitive short-day (SHORT DAY) birds (P > 0.05). Plasma LH of LAY hens peaked at 4.06 +/- 0.78 ng/ml from a prestimulation baseline of 2.30 +/- 0.21 ng/ml and that in NEST DEP birds increased from 1.08 +/- 0.18 ng/ml to 2.57 +/- 0.53 ng/ml. Administration of LHRH increased plasma LH levels in SHORT DAY, LAY, and NEST DEP hens with the increase being 2.0-, 2.5-, and 6.1-fold, respectively. Electrical stimulation in the median eminence increased plasma PRL (P < 0.05) in all the reproductive groups tested, with peak response being greatest for NEST DEP birds (661 +/- 126 ng/ml) followed by LAY (317 +/- 26 ng/ml), REFRAC (50 +/- 7 ng/ml), and SHORT DAY (39 +/- 12 ng/ml) hens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Dynorphin modulates prolactin secretion in the turkey.

Big dynorphin (prodynorphin 209-240), dynorphin A (prodynorphin 209-225), dynorphin B (prodynorphin 228-240), beta-endorphin (beta-lipotrophin 61-90), or Met-enkephalin, each infused into the third ventricle, were tested for their effect on PRL release in the anesthetized turkey hen. Laying hens that received big dynorphin at the rate of 0.35 nmol/min showed a 5.1-fold increase in serum PRL at the end of a 30-min infusion period. In a second experiment, the big dynorphin-induced PRL increase was 2.6-fold. Nest-deprived, previously incubating hens that received big dynorphin displayed an 8.2-fold increase in serum PRL. Laying and nest-deprived incubating control birds infused with saline displayed no PRL increases. Laying hens that received dynorphin A (0.35 nmol/min) showed a 1.5-fold increase in serum PRL after 30 min of infusion; after 40 min of infusion, this increase rose to 2.7-fold. Infusions of beta-endorphin (0.35 nmol/min), or Met-enkephalin (0.35 nmol/min) failed to evoke PRL increases in either laying or nest-deprived incubating turkeys. Infusion of big dynorphin or dynorphin A for 120 min maintained an elevated PRL level across the period, a level equal to that evoked by electrical stimulation of the medial preoptic nucleus (ES/POM). Infusion of dynorphin B (0.48 nmol/min) or a reduced dose of dynorphin A (0.09 nmol/min) augmented the PRL response evoked by ES/POM. No augmentation was noted for beta-endorphin or Met-enkephalin, nor for saline-infused controls. The dynorphin-induced PRL response appeared to be dose-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

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