close

Вход

Забыли?

вход по аккаунту

?

000127205

код для вставкиСкачать
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 [3], 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
[9]. 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
129.59.95.115 - 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 [14], VIP RIA was carried out by means of a
self-displacement double-antibedy RIA [15]. 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
129.59.95.115 - 10/27/2017 5:28:44 AM
er than inhibited, PRL secretion in nonlaying turkeys
[10]. 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 [11], DA is the major regulator of
PRL secretion in mammals via inhibitory Dy DA recep­
tors located on pituitary lactotropes [12], The D, DA
receptor has also been implicated in the stimulation of
mammalian PRL secretion [13], 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
129.59.95.115 - 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 [16]. 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 [17],
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
129.59.95.115 - 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
129.59.95.115 - 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 [25],
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 [26],
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 [27], 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 [3]. It is known
that the secretion of avian PRL also requires an intact
serotonergic system [28]. 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
129.59.95.115 - 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 [20], 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 [22], 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 [22], 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 [23]
and when the dopaminergic inhibition was abolished,
exogenous VIP was able to increase PRL secretion [24],
Previous results from intracranial infusion of the D 2
DA receptor antagonist and its effects on PRL secretion
were unclear [22], 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
129.59.95.115 - 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.
Документ
Категория
Без категории
Просмотров
2
Размер файла
1 462 Кб
Теги
000127205
1/--страниц
Пожаловаться на содержимое документа