C om p arative N e u ro e n d o c rin o lo g y -endocrinology Neuroendocrinology 1997:65:423-429 Yupaporn Chaiseha3 Orlan M. Youngrenb Mohamed E. El Halawania Dopamine Receptors Influence Vasoactive Intestinal Peptide Release from Turkey Hypothalamic Expiants Key W ords Abstract Vasoactive intestinal peptide Catecholamines Catecholamine receptor Birds 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 D| DA receptor antagonist (R+l-SCH-23390 HC1 completely negated the stimulatory effect of DA (100 nmol/min) upon VIP release. Perifusion with the Dy DA receptor antagonist S(-)-eticlopride HC1 by itself stim ulated 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 Di DA agonist (+)-SKF-38393 HC1 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 D t DA receptor agonist R(-)-NPA HC1 (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 D| and inhibitory Dy DA receptors in the turkey hypothalamus. Introduction It has been established for some time that prolactin (PRL) secretion in birds is tonically stimulated [1,2], and the factor responsible for this stimulation is vasoactive intestinal peptide (VIP), which originates from VIP neu rons located in the infundibular nuclear complex of the This is Scientific Journal Scries Paper 22.567 of the Minnesota Agriculture Experiment Station. Research supported by USDA grant No. 94-37203-0847. KA RCiFR IW \t\\J C l\ E-Mail kargcr(n karger .ch Pax + 4161 306 12 34 http://www.karger.ch © 1997 S. Karger AG, Basel OO28-3835/97/0656-O423S12.00/0 This article is also accessible online at: http://BioMcdNct.com/ktugcr hypothalamus , Several lines of evidence indicate that VIP is the avian PRL-releasing factor (PRF) [for reviews, see 4], In mammals, PRL secretion is primarily under tonic inhibitory control by dopamine (DA), which is released from the hypothalamus [5, 6]. DA inhibits PRL release in chicken and pigeon anterior pituitary cells in vitro [7, 8], Data from in vivo studies also support the concept that DA is inhibitory to the neuroendocrine sys tem which stimulates PRL secretion in laying turkey hens . However, other data suggest that DA stimulated, rath- Mohamed El Halawani 495 Animal Scicncc/Vcterinary Medicine. 1988 Fitch Avenue University of Minnesota St. Paul. MN 55108 (USA) Tel. (612) 624-9744. Fax (612) 625-2743 Downloaded by: Vanderbilt University Library 220.127.116.11 - 10/27/2017 5:28:44 AM Departments of a Animal Science and b Ecology, Evolution, and Behavior, University of Minnesota, St. Paul. Minn., USA Received: October 7.1996 Accepted after revision: February 18.1997 M aterials and M ethods Experimental Animats. Adult large white female Nicholas turkeys (weighing 8-10 kg) in their first reproductive cycle were used. They were reared and housed on a 15 h light: 9 h dark photoregimen, in temperature-controlled (15-21 °C) floor pens, with food and water continuously available. Hypothalami Preparation. After blood samples were taken, the birds were sacrificed by decapitation. The brain was immediately dissected intact from the skull, and the pituitary gland was detached under microscopic guidance to prevent any loss of median eminence tissue. The optic chiasma was dissected away from the ventral sur face of the brain to expose the underlying hypothalamus. A block of tissue limited rostrally by the septomcscncephalic tract and caudally by the posterior border of the mammillary bodies was removed. The block extended laterally 2 mm from the midline on each side. The block was 4 mm deep at its caudal end and 2 mm deep rostrally. This area included the median eminence, hypothalamus, and preoptic hypothalamus. The tissue block was sliced longitudinally twice on each side of the midline. The cuts did not extend all the way to the ends of the block, allowing the block to open up in an ‘accordion’ manner without separating into individual pieces. The explants were placed into ice-cold perifusion media before being transferred to the perifusion chambers. Perifusion Procedure. Each hypothalamus was transferred to a temperature-controlled perifusion chamber (500 pi volume) in a computer-guided perifusion system (APS-10; Endotronics, Coon Rapids, Minn., USA) consisting of 6 chambers running concurrently. Perifusate collected from the first 3 h of perifusion (flow rate 0.5 ml/ min) was discarded because of the variability in VIP secretion induced by initial tissue damage. The hypothalami were then peri fused continuously at a flow rate of 40 gl/min. The perifusion medium (at 41 °C) was constantly gassed with CCL-CF (5%/95%). 424 Neuroendocrinology 1997:65:423-429 5-min effluent fractions were collected into siliconized polypropy lene tubes, stored momentarily on ice, then kept at -8 0 °C until assayed for VIP. At the end of the experiment, tissue viability was demonstrated by adding 50 mM KC1 to the perifusion medium to depolarize the hypothalamic neurons. VIP concentrations were ex pressed as picograms VIP per 5 min. Perifusion Medium. Krebs-Ringer bicarbonate medium was used for perifusion with the following modifications: 10g/l crystalline bovine serum albumin (BSA, fraction V; Sigma, St. Louis, Mo., USA), 10 m M a-D(+(glucose (grade III: Sigma). 20 mA/ HEPES (Sig ma), 0.5 mM ascorbic acid (J.T. Baker Chemical, Phillipsburg, N.J., USA). 0.05 mM bacitracin (Aldrich, Milwaukee, Wise., USA), and 0.0056 mM phenol red (Sigma). The medium was then adjusted to pH 7.4. In the depolarizing medium, with elevated KC1 concentra tion (50 mM), NaCI concentration was reduced by an equimolar amount to maintain medium osmolality. Dopamine and Its Agonists or Antagonists. Dopamine hydrochlo ride (Sigma). D| DA receptor agonist (+)-SKF-38393 hydrochloride, selective Di DA receptor agonist R(-)-propylnorapomorphine hy drochloride. selective D| DA receptor antagonist R(+)-SCH-23390 hydrochloride, and selective D2 DA receptor antagonist S(-)-eticlopridc hydrochloride (Research Biochemicals International, Natick. Mass., USA) were used. They were dissolved in the perifusion medium immediately before use. During perifusion. the medium containing DA or its agonists or antagonists was protected from light with aluminium foil. VIP Radioimmunoassay (RIA). [(125I)Tryl0]VIP was prepared by the lodogen method , VIP RIA was carried out by means of a self-displacement double-antibedy RIA . All samples from the same experiment were assayed at the same time. The intraassay vari ation was 10%. The minimum detectable dose, based on 90% bound, was 0.2 pg/tube. PRL RIA. Serum PRL was determined according to the method of Proudman and Opel (1981). Serum PRL levels were determined to ensure that the birds were not hyper- or hypoprolactinémie. Average PRL value was 216.5 ± 43.5 ng/ml. Experimental Design and Analysis Experiment I: Effects o f DA upon VIP Release by Turkey Hypo thalamic Explants. Hypothalami of laying hens (n = 6) were sequen tially perifused with media alone or with media containing various concentrations of DA (10, 100, 1,000 nmol/min) at a flow rate of 40 pl/min. The hypothalami were perifused in three different modes. First, various concentrations of DA were delivered to the hypotha lamic fragments every 210 min in the following order: 40 min at 10 nmol/min DA, 40 min at 100 nmol/min DA and 40 min at 10 nmol/min DA. Second, DA was delivered in the following order: 40 min at 100 nmol/min every 210 min for three periods. Third, DA was delivered in the following order: 40 min at 1,000 nmol/min, 40 min at 100 nmol/min, and 40 min at 1,000 nmol/min every 210 min. After every 40-min DA perifusion. the hypothalamic frag ments were (lushed by perifusion media alone at the higher flow rate of 0.5 ml/min for 15 min to wash away residual DA. The perifusate was collected in 5-min aliquots in siliconized polypropylene tubes, held on ice momentarily, then stored at -80°C until assayed for VIP. Experiment 2: Effects o f Di DA Receptor Antagonist upon VIP Release by Turkey Hypothalamic Explants. The purpose of this Cha iseha/Youngrcn/El Halawan i Downloaded by: Vanderbilt University Library 18.104.22.168 - 10/27/2017 5:28:44 AM er than inhibited, PRL secretion in nonlaying turkeys . Recently, it has been shown that DA cither stimulat ed or inhibited PRL secretion in vivo, depending upon concentration, when infused into the third ventricle of the turkey brain. This infers possible biphasic actions for DA within the avian brain and suggests the existence of two different DA receptors to mediate the stimulatory and inhibitory responses , DA is the major regulator of PRL secretion in mammals via inhibitory Dy DA recep tors located on pituitary lactotropes , The D, DA receptor has also been implicated in the stimulation of mammalian PRL secretion , although its site of action has not been localized. The regulation of avian PRL secretion by DA is con troversial and remains largely unexplored, especially the interaction between the dopaminergic and VIPergic sys tems. The present study was conducted to investigate the involvement of DA in the regulation of VIP secretion util izing turkey hypothalamic explants perifused with DA and its agonists or antagonists. Experiment I: Effects o f DA upon VIP Release by Tur key Hypothalamic Explants. The addition of DA to the perifusion medium at concentrations of 10. 100 and 1.000 nmol/min for 40 min. resulted in a dose-dependent increase in basal VIP release from the hypothalamic explants. VIP increase in response to 10 nmol/min DA (from 67.2 ± 3.9 to 164.3 ± 3.1 pg/5 min), 100 nmol/min DA (from 70.1 ± 3.2 to 291.0 ± 7.5 pg/5 min), and 1.000 nmol/min DA (from 72.0 ± 4.8 to 501.0 ± 24.7 pg/ 5 min) differed significantly from basal VIP release (n = 6, p<0.05; fig. la-c). Experiment 2: Effect of D / DA Receptor Antagonist upon VIP Release by Turkey Hypothalamic Explants. As in experiment 1. perifusion of the explants (n = 6) with DA (100 nmol/min) increased VIP release from 56.4 ± 2.7 to 242.7 ± 26.9 pg/5 min (p < 0.05; fig. 2a). Perifu sion of D| DA receptor antagonist (100 nmol/min) for 90 min produced no effect on basal VIP release from the hypothalami. Prior perifusion with the Di DA antagonist completely negated the stimulatory effect of DA (100 nmol), reducing VIP from 242.7 ± 26.9 to 50.3 ± 3.3 pg/5 min (n = 6. p < 0.05; fig. 2a). Experiment 3: Effects of D2 DA Receptor Antagonist upon VIP Release by Turkey Hypothalamic Explants. Per ifusion of hypothalamic fragments (n = 6) with the Dy DA receptor antagonist (100 nmol/min) for 90 min signifi cantly increased (p < 0.05) basal VIP release (from 38.1 + 5.3 to 161.9 ± 9.7 pg/5 min) and the pulse amplitude (from 17.8 ± 2.5 to 87.4 ± 16.6 pg/5 min) without chang ing other mean pulse characteristics. VIP release re mained elevated throughout the perifusion period with the D t DA receptor antagonist (fig. 2b). Subsequent peri fusion of DA (100 nmol/min) in combination with the D t DA antagonist (100 nmol/min) caused no significant al teration (n = 6, p > 0.05) in ongoing VIP release (161.9 ± 9.7 vs. 154.1 ± 11.7 pg/5 min) after 30 min. Experiment 4: Effects o f Dt DA Agonist upon VIP Release by Turkey Hypothalamic Explants. Consistent with the hypothesis that D| DA receptors regulate VIP release, the D| DA receptor agonist (100 nmol/min) sig nificantly increased the basal VIP release from 44.9 ± 4.4 to 151.3 ± 9.3 pg/5 min after 180 min (n = 6, p < 0.05; data not shown). Mean pulse amplitude of VIP release increased from 28.6 ± 3.8 to 56.3 ± 4.7 pg/5 min (n = 6. p < 0.05; data not shown), but other pulse characteristics did not differ. Experiment 5: Effects o fD 1 DA Agonist and/or I f DA Agonist upon VIP Release by Turkey Hypothalamic Explants. As in experiment 4, challenge of hypothalamic explants (n = 6) with the D| DA receptor agonist (100 nmol/min) for 180 min dramatically increased VIP release from 52.7 ± 4.6 to 192.6 ± 16.9 pg/5 min (p < 0.05; fig. 3). Perifusion with the D t DA receptor agonist (100 nmol/min) for 90 min produced no significant effect upon VIP release (72.1 ± 5.7 vs. 92.9 ± 4.1 pg/5 min; p> 0.05). The perifusion of the D t DA agonist in combina tion with the D| DA agonist partially inhibited the stimu latory effect of the D, DA agonist upon basal VIP release (from 192.6 ± 16.9 to 139.65 ± 1 3 . 8 pg/5 min; n = 6, p < 0.05). The mean pulse amplitude decreased significantly from 90.5 ± 9.3 to 60.4 ± 7.6 pg/5 min. Dopaminergic Mediation of Avian VIP Ncurocndocrinology 1997:65:423-429 Results 425 Downloaded by: Vanderbilt University Library 22.214.171.124 - 10/27/2017 5:28:44 AM experiment was to determine if DA-induced VIP release was me diated through D| DA receptors. Hypothalamic fragments from 6 laying hens were perifused sequentially with media alone, with media containing lOOnmol/min DA. or with media containing D| DA antagonist (100 nmol/min). The hypothalami were perifused in the following order: 210 min with medium alone. 30 min with 100 nmol/ min DA, 120 min with medium alone, 90 min with 100 nmol/min Di DA antagonist, 30 min with 100 nmol/min D| DA antagonist plus 100 nmol/min DA, and 120 min with medium alone. After each drug challenge, the hypothalamic fragments were Hushed to remove resid ual DA and D| DA antagonist from the perifusion chambers as described in experiment I. Experiment 3: Effects o f D? DA Receptor Antagonist upon VIP Release by Turkey Hypothalamic Explants. This experiment was designed to determine if DA-induced VIP release was mediated via D 2 DA receptors. The sequence of treatments was the same as in experiment 2, except that the explants received a D? DA antagonist (100 nmol/min) instead of a D| DA antagonist. Experiment 4: Effects o f D, DA Agonist upon VIP Release by Tur key Hypothalamic Explants. Hypothalami were taken from 6 laying hens and sequentially perifused in the following order: 210 min with medium alone. 180 min with D| DA agonist (100 nmol/min), and 180 min with medium alone. Experiment 5: Effects o f D/ DA Agonist and/or D j DA Agonist upon VIP Release by Turkey Hypothalamic Explants. Hypothalami from 6 laying hens were perifused with media containing a D| DA agonist alone or with a combination of D| and D t DA agonist. The explants were perifused in the following order: 180 min with medium alone, 180 min with D t DA agonist (100 nmol/min), 60 min with medium alone, 90 min with D; DA agonist (100 nmol/min), 180 min with D t DA agonist plus D) DA agonist, and 90 min with medium alone. Statistical Analysis. VIP secretory patterns were analyzed em ploying PC Pulsar Software . The cut-off criteria for peak identi fication were G (l) = 3.80. G(2) = 2.60, G(3)= 1.90, G(4)= 1.50. and G(5) = 1.20. Mean pulse amplitude, peak length, pulse frequency, and peak interval were determined for each explant. The significant differences in VIP release were analyzed utilizing the General Linear Model (GLM) procedure in the Statistical Analysis System , Duncan's multiple range test was used to analyze the differences in VIP release among treatment groups. A p value of < 0.05 was consid ered as statistically significant. 500 10 n m o le 1 00 n m o le 10 n m o le 400 300 200 100 __ 0 500 1 00 n m o le 1 00 n m o le 1 00 n m o le 400 E 300 in O) a a. Jj 200 > 100 ' Fig. 1. a-c Representative individual graphs illustrating stimulatory effects of DA (10. 100. and 1,000 nmol) and 50 mM KCI upon the VIP release from turkey hypotha lamic explants. D iscu ssio n The present study clearly demonstrated that DA stim ulated VIP release from the turkey hypothalamus and did so in a dose-dependent manner. The amplitude of the VIP pulse was increased during every DA challenge and the 426 Neurocndocrinology 1997:65:423-429 1 ! TIM E(m in) amount of VIP released was dependent upon the DA con centration. Furthermore, the stimulatory effect of DA upon VIP release could be mimicked by perifusing the hypothalamus with a D| DA receptor agonist and totally negated by blockade of the Di DA receptors. Perifusion of the hypothalamus with a D 2 DA receptor agonist was Chaiseha/Youngren/El Halawani Downloaded by: Vanderbilt University Library 126.96.36.199 - 10/27/2017 5:28:44 AM 0 400 DA c 300 ■ I E in 0 )2 0 0 Q. ' J Q. > 100 Fig. 2. a Representative individual plots showing the effect of DA (100 nmol), the selective D| DA receptor antagonist, R(+)SCH-23390 HC1 (100 nmol), the combina tion of DA and D| DA antagonist, and 50 mM KC1 upon VIP release from turkey hypothalamic explants, b Representative in dividual plots of VIP release from turkey hypothalamic explants in response to chal lenge by DA (100 nmol), the selective D2 DA receptor antagonist, S(-)-eticlopride HC1 (100 nmol) or the combination of DA and D2 DA antagonist. 0 100 200 300 400 500 600 700 800 T IM E (m in ) 400 |D - —góñíst ; D1 A G O N IST d^ gonist 60 0 700 I c 300 E m 0 )2 0 0 Q. Q- > 100 VIP release in response to D| DA receptor agonist (100 nmol) or the combination of Dj DA agonist and D2 DA agonist (100 nmol). Dopaminergic Mediation of Avian VIP 100 200 30 0 400 500 800 900 T IM E (m in ) Neuroendocrinology 1997;65:423-429 427 Downloaded by: Vanderbilt University Library 188.8.131.52 - 10/27/2017 5:28:44 AM Fig. 3. Representative individual plots of 428 Neuroendocrinology 1997:65:423-429 PRL mRNA levels in turkey pituitary cell cultures , indicating the presence of D2 DA receptors within the tur key pituitary. Unpublished data from our laboratory have indicated that both high and low concentrations of DA inhibited PRL secretion when infused directly into the anterior pituitary of the turkey. This would suggest that the major site of action for DA inhibition of PRL is not in the avian hypothalamus, but in the pituitary. Very few anatomical data concerning the cellular local ization of DA receptors are available in birds. The exis tence of specific DA-binding sites has been identified in the anterior and posterior hypothalamus of the hen , Recently, three genomic clones encoding D|-Iike DA receptors have been isolated from the chicken hypothala mus, named D|A. D|B, and D |D , In the quail brain, the D| DA-like receptor density was shown to be low but significantly detectable in the preoptic area and other parts of the hypothalamus, such as the infundibulum [21 ], where abundant VIP neurons are present . It is known that the secretion of avian PRL also requires an intact serotonergic system . These findings taken together suggest the involvement of a complex and even redundant network in PRL control, where an integrative interaction among VIPergic, dopaminergic, and serotonergic systems exerts a stimulatory effect upon PRL secretion. In summary, the present data clearly demonstrated that DA stimulated VIP release from perifused turkey hypothalami in a dose-dependent manner, and that this release was totally abolished by blocking the D) DA recep tor. Similarly, VIP release due to DA was mimicked by a D, DA agonist. The stimulatory effects of the Di DA ago nist upon VIP release was partially inhibited by the D 2 DA agonist. These results suggest that VIP secretion is, in part, regulated by the relative activities of stimulatory Di and inhibitory D2 DA receptors within the turkey hypo thalamus. Chaischa/Youngren/El Halawani Downloaded by: Vanderbilt University Library 184.108.40.206 - 10/27/2017 5:28:44 AM without effect, indicating that stimulation of D2 DA receptors did not cause an increase in VIP release. These results suggest that DA stimulates VIP release via phar macologically characterized Dj-like dopaminergic recep tors that exist in the turkey hypothalamus. D r like DA receptors have been mapped in the brain of the pigeon [18, 19], the European starling , and the quail [21 ] by autoradiography. The in vitro results of the current study correspond nicely with the in vivo finding that stimula tion of turkey PRL secretion by DA was mediated central ly through D| DA receptors , When these receptors were blocked, PRL release could no longer be stimulated by intracranial infusion of DA. In addition, the presence of VIP was needed in order for DA to stimulate PRL secretion. In turkeys actively immunized against VIP. intracranial infusions of DA were ineffective in releasing PRL, suggesting that DA affects PRL secretion by stimu lating the release of VIP , There is evidence that DA and VIP from exogenous or hypothalamic sources are involved in the regulation of PRL secretion in mammals, each of them acting on pituitary lactotropes. Dopamine blocked the VIP-induced PRL response in women  and when the dopaminergic inhibition was abolished, exogenous VIP was able to increase PRL secretion , Previous results from intracranial infusion of the D 2 DA receptor antagonist and its effects on PRL secretion were unclear , Low doses of the drug (0.1, 1.0, 10.0 nmol/min) had no effect, while the highest concen tration (100 nmol/min) produced an increase in circulat ing PRL. Similarly, in the present study, VIP basal release gradually increased and was maintained at high levels when turkey hypothalami were perifused with 100 nmol/ min D: DA receptor antagonist. The interpretation of this finding is difficult and speculative at best, since high con centrations of the drug may be affecting VIP secretion by acting as a partial agonist toward D| DA receptors or affecting other cell parameters, such as ion channels. Nev ertheless, the reduction in D| DA receptor agonist-stimu lated VIP secretion induced by the D2 DA receptor ago nist suggests that both D| and D2 receptors are present in the turkey hypothalamus. The quantity of VIP released may be due to a balance between relative activities of stimulatory D| and inhibitory D 2 DA receptors. As pre viously demonstrated [11, 22], DA had both stimulatory and inhibitory effects on turkey PRL secretion, suggesting the existence of different DA receptors to mediate the stimulatory and inhibitory responses. However, in the present perifusion study, both high and low DA concen trations were stimulatory for VIP release. D2 DA receptor agonists have been shown to inhibit PRL secretion and References Dopaminergic Mediation of Avian VIP 11 Youngren OM. Pitts GR. Phillips RE. El Hala wani ME: The stimulatory and inhibitory ef fects of dopamine on prolactin secretion in the turkey. Gen Comp Endocrinol 1995:98:111— 117. 12 Civclli O. Bunzow JR. Grandy DK. Zhou Q-Y. VanTol HHM: Molecular biology of the dopa mine receptors. Eur J Pharmacol 1991:207: 277-286. 13 Porter TE. Grandy D, Bunzow J. Wiles CD, Civelli O. Frawley LS: Evidence that stimulato ry dopamine receptors may be involved in the regulation of prolactin secretion. Endocrinolo gy 1994:134:1263-1268. 14 McMaster D. Suzuki Y. Rostad O. Lederis K: Iodinated derivatives of vasoactive intestinal peptide (VIP). PHI and PHM: Purification, chemical characterization and biological activi ty. Peptides 1987:8:663-676. 15 Mauro LI, Youngren OM, Proudman JA. Phil lips RE, El Halawani ME: Effects of reproduc tive status, ovariectomy, and photoperiod on vasoactive intestinal peptide in the female tur key hypothalamus. Gen Comp Endocrinol 1992:87:481-493. 16 Gitzen JF. Ramirez VD: PC-Pulsar-Pulsar for the IBM-PC: Operating Instructions. Version 3.0. Distributed with the PC-Pulsar Program. 1989. 17 SAS Institute: SAS/STAT User’s Guide. Ver sion 6. cd 4. Cary SAS. Institute Inc, 1989. 18 Dietl MM. Palacios JM: Neurotransmitters in the avian brain. 1. Dopamine receptors. Brain Res 1988:439:354-359. 19 Richfield EK. Young AB. Penny JB: Compara tive distribution of dopamine D| and Dj recep tors in the basal ganglia of turtles, pigeons, rats, cats, and monkeys. J Comp Neurol I987;262: 446-463. 20 Casto JM. Ball GF: Characterization and local ization of D | dopamine receptors in the sexual ly dimorphic vocal control nucleus, area X. and the basal ganglia of European starlings. J Ncu robiol 1994;25:767-780. 21 Ball GF. Casto JM. Balthazart J: Autoradio graphic localization of D|-likc dopamine recep tors in the forebrain of male and female Japa nese quail and their relationship with immunoreactivc tyrosine hydroxylase. J Chcm Neuroanat 1995:9:121-133. 22 Youngren OM. Pitts GR. Phillips RE. El Hala wani ME: Dopaminergic control of prolactin secretion in the turkey. Gen Comp Endocrinol 1996:104:225-230. 23 Conti A. Togni E. Travaglini P, Muratori M, Faglia G: Vasoactive intestinal polypeptide and dopamine: Effect on prolactin secretion in normal women and patients with microprolac tinomas. Neuroendocrinology 1987:46:241 — 245. 24 Rostenc WH. Charpentier G: Peptide and amine interactions in central nervous system and pituitary functions: Functional and clinical aspects: in Labric F. Proulx L (eds); Endocri nology Int Congr Ser No 655. Amsterdam. Excerpta Medica, 1984. pp 1007-1012. 25 Xu M. Proudman J A. Pitts GR. Wong EA, Fos ter DN. El Halawani ME: Vasoactive intestinal peptide stimulates prolactin mRNA expression in turkey pituitary cell: Effects of dopaminergic drugs. Proc Soc Exp Biol Med 1996:212:5262. 26 Macnamee MC. Sharp PJ: The functional ac tivity of hypothalamic dopamine in broody bantam hens. J Endocrinol 1989; 121:67—74. 27 Dcmchyshyn LL. Sugamori KS. Lee FJS. Hamadanizadeh SA. Niznik HB: Cloning and characterization of three pharmacologically distinct Dplikc receptors from Gallus domesticus. J Biol Chem 1995:270:4005-4012. 28 El Halawani ME. FehrerSC, HargisBH. Porter TE: Incubation behavior in the domestic tur key: Physiological correlates. CRC Crit Rev Poult Biol 1988:1:285-314. Neuroendocrinology 1997:65:423-429 429 Downloaded by: Vanderbilt University Library 220.127.116.11 - 10/27/2017 5:28:44 AM 1 Bern HA. Nicoll CS: The comparative endocri nology of prolactin. Recent Prog Horrn Res 1968:24:681-720. 2 Kragt CL, Meities J: Stimulation of pigeon pituitary prolactin release by pigeon hypotha lamic extract in vitro. Endocrinology 1965:76: 1169-1176. 3 Mauro U . Elde RP. Youngren OM, Phillips RE, El Halawani ME: Alterations in hypotha lamic vasoactive intestinal peptide-like immunoreactivitv arc associated with reproduction and prolactin release in the female turkey. En docrinology 1989:125:1795-1804. 4 El Halawani ME. Youngren OM. Pitts GR: Vasoactive intestinal peptide as the avian pro lactin releasing factor, in Etches R. Harvey S (eds): Prospective in Avian Endocrinology. Bristol, Society of Endocrinology, in press. 5 Lamberts SWJ, Maclcod RM: Regulation of prolactin secretion at the level of the lactotroph. Physiol Rev 1990;70:279-318. 6 Ben-Jonathan N, Arbogast LA. Hyde JF: Neu roendocrine regulation of prolactin release. Prog Ncurobiol 1989:33:339-447. 7 Hall TR. Chadwick A: Hypothalamic control of prolactin and growth hormone secretion in the pituitary gland o f the pigeon and the chick en: In vivo studies. Gen Comp Endocrinol 1983;49:135-143. 8 Hall TR. Chadwick A: Dopaminergic inhibi tion of prolactin release from pituitary glands of the domestic fowl incubated in vitro. J Endo crinol 1984:103:63-69. 9 El Halawani ME. Youngren OM. Silsby JL. Phillips RE: Involvement of dopamine in pro lactin release induced by electrical stimulation of the hypothalamus of the female turkey (Meleagrisgalloparo). Gen Comp Endocrinol 1991; 72:323-328. 10 Hargis BM. Burke WH: Influence of cerebroventricular injection of dopamine on plasma prolactin and LH levels of post-laying and broody turkey hens. Gen Comp Endocrinol 1986;61:142-147.