Download Serum Concentrations of Luteinizing Hormone, Growth Hormone

Serum Concentrations of Luteinizing Hormone, Growth Hormone, and
Cortisol in Gilts Treated with N-Methyl-D,L-Aspartate During the
Estrous Cycle or After Ovariectomy1
M. J. Estienne*,2, W. F. Hurlock*,3, and C. R. Barb†
*Department of Agriculture, University of Maryland Eastern Shore, Princess Anne 21853 and
†Animal Physiology Unit, ARS, USDA, Athens, GA 30613
ABSTRACT:
The objective of this experiment was
to determine the effects of n-methyl-d,l-aspartate
(NMA), an agonist of the neurotransmitter glutamate, on circulating concentrations of LH, GH, and
cortisol in gilts treated during the luteal ( n = 4 ) or
follicular ( n = 4 ) phase of the estrous cycle, or after
ovariectomy ( n = 4). Blood was sampled every 15 min
for 10 h on each of two consecutive days. On the 1st d,
two gilts from each group received i.v. injections of
NMA (10 mg/kg BW) at h 4 and 6, and the remaining
gilts received .9% saline (vehicle). The following day,
gilts that had received NMA on the 1st d received
vehicle, and gilts that had received vehicle on d 1
received NMA. All gilts received an i.v. challenge of
GnRH (.1 mg/kg BW) at h 8 on each day. The NMA
treatment increased ( P < .01) LH pulse frequency in
luteal-phase gilts by 125%. In contrast, NMA
decreased ( P < .05) mean concentrations of LH by
48% and suppressed ( P < .01) LH pulse frequency by
33% in ovariectomized gilts. No characteristics of LH
secretion were affected ( P > .05) by NMA in follicular
phase gilts. Serum LH concentrations for the
2-h period following GnRH were lower ( P < .05) in
follicular-phase gilts than in ovariectomized gilts and
were 1.15 ± .09 (mean ± SE), .81 ± .05, and .51 ± .17
ng/mL for ovariectomized, luteal-phase, and follicularphase gilts, respectively. Treatment with NMA increased circulating concentrations of GH by 334% ( P <
.01) and cortisol by 77% ( P < .03) in all gilts. We
suggest that the effects of NMA on LH release in gilts
depend on the circulating steroidal milieu. In contrast,
NMA evokes secretion of GH and cortisol irrespective
of the reproductive status of treated gilts.
Key Words: LH, Somatotropin, Hydrocortisone, Neurotransmitters, Gilts
1998 American Society of Animal Science. All rights reserved.
Introduction
Evidence suggests that glutamate, acting like a
classical neurotransmitter, participates in neuroendocrine function and influences secretion of LH from the
anterior pituitary gland in mammals (Brann et al.,
1This research was supported by the Maryland Pork Producers
Assoc., the USDA 1890 Capacity Building Grant Program, and
Evans Allen Funds allocated to the Univ. of Maryland Eastern
Shore. The authors wish to express sincere gratitude to S. Bishop, V.
Cotton, and W. Douet and to B. Barrett, M. Stott, L. Baker, J.
Popwell, and N. Whitley for their expert assistance with animal care
and with laboratory analyses, respectively. The authors thank D. J.
Bolt, ARS, USDA, Beltsville, MD, and A. F. Parlow, Harbor-UCLA
Medical Center, Torrance, CA, for providing pituitary hormones,
and antisera, respectively.
2To whom correspondence should be addressed: phone:
410-651-6194; fax: 410-651-6207.
3Current address: Wayne Farms, P.O. Box 470, Union Springs,
AL 36089.
Received December 30, 1997.
Accepted April 10, 1998.
J. Anim. Sci. 1998. 76:2162–2168
1996). Sesti and Britt (1992) reported that i.v.
injections of n-methyl-d,l-aspartate ( NMA) , a potent
agonist of glutamate, increased LH secretion in
lactating sows and ovariectomized, estradiol-treated
gilts. A stimulatory effect of NMA on LH secretion was
also demonstrated in our laboratory, using prepubertal gilts as the experimental animals (Estienne et al.,
1995). Consistent with a central site of action for
NMA, administration of GnRH antisera to ovariectomized gilts abolished the ability of the compound to
increase LH secretion (Sesti and Britt, 1992).
In contrast, Barb et al. (1992) and Chang et al.
(1993) reported that NMA was ineffectual in altering
LH secretion in ovariectomized, estradiol-treated gilts
and that it decreased LH release in ovariectomized,
progesterone-treated gilts. These steroid treatments
were used to establish, in ovariectomized gilts, circulating concentrations of steroids that mimicked
those of the follicular (high estradiol) and luteal
(high progesterone) phases of the estrous cycle.
However, the effect of NMA on LH release in gilts
during an actual estrous cycle has not been reported.
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ENDOCRINE RESPONSES TO N-METHYL-D,L-ASPARTATE
Thus, in an effort to assess the role of glutamate in
neuroendocrine regulation of pituitary hormone secretion, circulating concentrations of LH, GH, and
cortisol were determined in gilts treated with NMA
during the luteal and follicular phases of the estrous
cycle or after ovariectomy.
Materials and Methods
Animals. The experiment was conducted at the
University of Maryland Eastern Shore ( UMES)
Swine Research and Education Facility in Princess
Anne, and the experimental protocol was approved by
the UMES Institutional Animal Care and Use Committee. Prepubertal Poland China × Yorkshire gilts ( n
= 18) were given an i.m. injection of 400 IU of PMSG
and 200 IU of hCG (P.G. 600, Intervet, Millsboro,
DE). Seventeen gilts (94%) displayed standing estrus
within 7 d after P.G. 600 treatment, and 13 gilts
(72%) displayed a second estrus approximately 21 d
later. Eight gilts that displayed a second estrus were
then used for the experiment. The injections of P.G.
600 were staggered such that during the experiment
gilts were in either the luteal ( 8 to 11 d after onset of
estrus; n = 4 ) or follicular (17 to 20 d after onset of
estrus; n = 4 ) phase of the estrous cycle. An additional
four gilts were ovariectomized via midventral
laparotomy 2 wk before the experiment. On the day
before the experiment, all gilts were fitted with
indwelling jugular vein catheters (Kraeling et al.,
1982), which were used for collecting sequential blood
samples and for administering NMA.
At the time of the experiment, selected gilts were
approximately 200 d of age and weighed an average of
122 kg. Gilts were individually penned (3.94 m2
totally slatted floor space/pen) in a passively ventilated, curtain-sided finishing barn. Average temperature was 20°C, and animals were exposed to the
natural photoperiod for mid-August. Gilts were allowed ad libitum access to a fortified, corn-soybean
meal pelleted diet (16% crude protein; Southern
States Cooperative, Baltimore, MD) and to water.
Experimental Protocol. Blood was sampled every 15
min for 10 h on each of two consecutive days. On the
1st d, two gilts from each group (i.e., luteal phase,
follicular phase, or ovariectomized) received i.v. injections of NMA (Sigma Chemical Co., St. Louis, MO; 10
mg/kg BW) at h 4 and 6, and the remaining animals
received .9% saline (vehicle). The dose of NMA used
was previously shown to increase concentrations of LH
in serum of prepubertal gilts (Estienne et al., 1995).
On the following day, gilts that received NMA on the
1st d received vehicle, and gilts that had received
vehicle on d 1 received NMA. All gilts received an i.v.
challenge of GnRH (acetate salt; Sigma; .1 mg/kg BW
dissolved in .9% saline) at h 8 on each day.
Blood Handling Procedures and Radioimmunoassays.
Blood samples were allowed to clot overnight at 4°C.
2163
Serum was collected and stored at −20°C until
assayed. All samples were analyzed to determine
serum LH concentrations with a specific RIA (Kesner
et al., 1987). Intra- and interassay CV were 13.6 and
7.5%, respectively. Assay sensitivity was .15 ng/mL.
Samples collected from h 0 to 8 were analyzed for
GH using a previously reported procedure (Barb et
al., 1991). Intra-and interassay CV were 2.1 and 1.3%,
respectively, and assay sensitivity was .4 ng/mL.
Samples collected from h 3 to 8 were analyzed for
serum cortisol concentrations as previously reported
(Barb et al., 1992). Intra- and interassay CV were 3.0
and 1.5%, respectively, and assay sensitivity averaged
1.0 ng/mL.
The first samples collected on each day were
analyzed for serum progesterone and estradiol concentrations using commercially available kits (Diagnostic
Systems Laboratories, Webster, TX), validated for
porcine serum in our laboratory. For the progesterone
assay, parallelism was demonstrated by showing that
estimates of progesterone concentrations were not
influenced by volume of serum assayed (.4 to 25 mL).
Recovery of .2, 7, or 9.1 ng of added progesterone
averaged 92.6%. Assay sensitivity was .3 ng/mL,
corresponding to 90% maximum binding of the label.
The intraassay CV, determined by replicating a single
serum pool containing 8.4 ng progesterone/mL twice in
a single assay, was 13.6%.
Parallelism of the estradiol assay was demonstrated
by showing that estimates of estradiol concentrations
were not influenced by volume of serum assayed (25
to 200 mL). Recovery of 4.7 or 280.1 pg of added
estradiol averaged 101.2%. Assay sensitivity averaged
3.4 pg/mL, which corresponded to 90% maximum
binding of the label. The intra- and interassay CV
determined by replicating a single serum pool containing 5.1 pg of estradiol/mL four times in two assays
were 11.7 and 22.0%, respectively.
Statistical Analyses. Mean concentrations of LH,
GH, and cortisol and the frequency and amplitude of
LH pulses were calculated for the period before the
first NMA or saline injection and the 4-h period after
the first NMA or saline injection (i.e., h 4 to 8 ) for
each gilt. A LH pulse was defined as an increment
greater than the intraassay CV that occurred within
30 min after the previous nadir (Estienne et al.,
1989). Pulse amplitude was defined as the difference
between the pulse peak and the preceding nadir.
Data were then subjected to ANOVA. The statistical model included treatment (NMA or saline),
reproductive status (luteal, follicular, or ovariectomized), period (before or after initiation of NMA or
saline injections), treatment × period, and treatment ×
period × reproductive status as possible sources of
variation. If significant three-way interactions were
detected, additional one-way ANOVA were conducted
to determine the effects of period within treatment
and reproductive status. When treatment × period was
significant, additional one-way ANOVA were con-
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ESTIENNE ET AL.
ducted to determine the effects of period within
treatment (Gill and Hafs, 1971).
Concentrations of LH that followed the GnRH
challenge at h 8 were compared using ANOVA. The
model included treatment, reproductive status, and
treatment × reproductive status as possible sources of
variation. Means for the three reproductive statuses
were compared using Tukey’s studentized range test.
Results
One gilt that was classified as being in the follicular
phase based on day of the estrous cycle had serum
progesterone (6.55 ng/mL) and estradiol concentrations (below assay sensitivity) consistent with a
luteal-phase gilt. This gilt was not included in the
statistical analyses. Serum progesterone concentrations in the remaining luteal-phase animals were 8.11
± 1.13 ng/mL (mean ± SE) and were undetectable in
the follicular-phase and the ovariectomized gilts.
Serum concentrations of estradiol were 5.38 ± 2.33 pg/
mL for follicular-phase gilts and were undetectable for
luteal-phase and ovariectomized gilts.
There was an effect ( P < .03) of treatment × period
× reproductive status on mean LH concentrations
(Figure 1). Before the injections, mean LH concentrations were .69 ± .07, .27 ± .02, and .24 ± .05 ng/mL for
ovariectomized, luteal-phase, and follicular-phase
gilts, respectively. Injections of saline had no effect ( P
> .05) on mean LH concentrations in any group.
Injections of NMA decreased ( P < .05) mean concentrations of LH in ovariectomized gilts by 48%.
Treatment with NMA had no effect ( P > .05) on mean
concentrations of LH in luteal- or follicular-phase
gilts.
The frequency of LH pulses before and after NMA
or saline in ovariectomized, luteal-phase, and follicular-phase gilts is depicted in Figure 2. There was an
effect ( P < .01) of treatment × period × reproductive
status. Before the initiation of NMA and saline
injections, LH pulse frequencies were 5.25 ± .16, .88 ±
.12, and 1.52 ± .28 pulses/4 h for ovariectomized,
luteal-phase, and follicular-phase gilts, respectively.
Injections of saline had no effect ( P > .05) on LH pulse
frequency in any group. Injections of NMA decreased
( P < .01) LH pulse frequency by 33% in ovariectomized gilts and increased ( P < .01) the frequency of
LH pulses in luteal-phase gilts by 125%. An LH
secretory episode identified as a pulse immediately
followed every injection of NMA in luteal-phase gilts.
In contrast, NMA had no effect ( P > .05) on LH pulse
frequency in follicular-phase gilts.
There were no effects ( P > .05) of treatment,
treatment × period, or treatment × period × reproductive status on the amplitude of LH pulses. Amplitude
of LH pulses was .36 ± .01 ng/mL for ovariectomized
gilts, .55 ± .28 ng/mL for luteal-phase gilts, and .18 ±
.02 ng/mL for follicular-phase gilts (effect of reproduc-
Figure 1. Mean LH concentrations in serum of
ovariectomized (OVX; n = 4), luteal phase (n = 4), and
follicular phase (n = 3) gilts before (⁄; h 0 to 4) and
during (◊; h 4 to 8) n-methyl-d,l-aspartate (NMA) or
saline treatment. Blood samples were collected at
15-min intervals throughout the experiment, and NMA
and saline were injected at h 4 and 6. Values are means ±
SE. Injections of NMA decreased (P < .05; *) mean
concentrations of LH by 48% in OVX gilts. In contrast,
injections of NMA had no effect (P > .05) on mean LH
concentrations in luteal or follicular phase gilts.
tive status, P < .01). The LH pulse amplitude was
higher before injections of NMA or saline (.43 ± .06
ng/mL) than after them (.32 ± .03 ng/mL; effect of
period, P < .04).
Serum LH profiles from h 0 to 8 for individual,
NMA-treated ovariectomized, luteal-phase, and follicular-phase gilts are shown in Figures 3, 4, and 5,
respectively.
ENDOCRINE RESPONSES TO N-METHYL-D,L-ASPARTATE
2165
Figure 3. Serum LH concentrations in a representative, ovariectomized gilt. Blood samples were collected
at 15-min intervals, and n-methyl-d,l-aspartate (NMA;
10 mg/kg BW) was injected i.v. at h 4 and 6
(represented by the vertical arrows).
ovariectomized gilts and were 1.15 ± .09, .81 ± .05, and
.51 ± .17 ng/mL for ovariectomized, luteal-phase, and
follicular-phase gilts, respectively. Maximum serum
concentrations of LH following GnRH were lower ( P <
.05) in follicular-phase than in ovariectomized gilts
and were 2.07 ± .16, 1.60 ± .09, and .77 ± .21 ng/mL for
ovariectomized, luteal-phase, and follicular-phase
gilts, respectively.
Mean serum concentrations of GH and cortisol for
gilts treated with NMA or saline appear in Table 1.
There was no effect ( P > .05) of treatment × period ×
reproductive status for mean serum concentrations of
Figure 2. Frequency of LH pulses in ovariectomized
(OVX; n = 4), luteal phase (n = 4), and follicular phase (n
= 3) gilts before (⁄; h 0 to 4) and during (◊; h 4 to 8) nmethyl-d,l-aspartate (NMA) or saline treatment. Blood
samples were collected at 15-min intervals throughout
the experiment, and NMA and saline were injected at h
4 and 6. Values are means ± SE. Injections of NMA
increased (P < .01; **) LH pulse frequency in luteal
phase gilts by 125% and decreased (P < .01; **) LH pulse
frequency in OVX gilts by 33%. In contrast, NMA had
no effect (P > .05) on LH pulse frequency in follicular
phase gilts.
There was an effect ( P < .01) of reproductive status
but no effects ( P > .05) of treatment or treatment ×
reproductive status on serum concentrations of LH for
the 2-h period following the GnRH challenge or on
maximum LH levels after administration of GnRH.
Serum LH concentrations for the 2-h period following
GnRH were lower ( P < .05) in follicular-phase than in
Figure 4. Serum LH concentrations in a representative, luteal phase gilt. Blood samples were collected at
15-min intervals, and n-methyl-d,l-aspartate (NMA; 10
mg/kg BW) was injected i.v. at h 4 and 6 (represented
by the vertical arrows).
2166
ESTIENNE ET AL.
Figure 5. Serum LH concentrations in a representative, follicular phase gilt. Blood samples were collected
at 15-min intervals, and n-methyl-d,l-aspartate (NMA;
10 mg/kg BW) was injected i.v. at h 4 and 6
(represented by the vertical arrows).
either hormone. There was, however, an effect of
treatment × period for mean GH ( P < .01) and cortisol
( P < .04) concentrations. Injections of saline had no
effect ( P > .05) on GH and cortisol levels. Treatment
with NMA, however, increased serum concentrations
of GH by 334% ( P < .01) and cortisol by 77% ( P < .03)
in all gilts.
Behavior of Gilts Following Administration of NMA.
Gilts receiving injections of .9% saline displayed no
noticeable behavioral changes. In contrast, injections
of NMA caused vomiting.
Discussion
A group of amino acids that includes glutamate and
aspartate and that are collectively referred to as the
excitatory amino acids satisfy the main criteria for
classification as neurotransmitters (van den Pol et al.,
1996). Glutamate and aspartate, and receptors for
these excitatory amino acids, are ubiquitously distributed in the brain and are in the hypothalamus and
median eminence in many species (Petralia and
Wenthold, 1996). There are several types of receptors
that are stimulated by glutamate, and these are
named according to their selective agonists. Receptor
types
include
n-methyl-d-aspartate
( NMDA) ,
kainate, and d,l-amino-3-hydroxy-5-methyl-4-isoxazole
propionic acid ( AMPA) (Petralia and Wenthold,
1996). The excitatory amino acids may be the major
neurotransmitters in the mammalian central nervous
system and play a paramount role in the neuroendocrine control of anterior pituitary gland function.
For swine, there is no information on the effects of
kainate and AMPA receptor stimulation on secretion
of LH. However, NMA is a potent agonist of the
NMDA receptor and has been demonstrated to stimulate secretion of LH in lactating sows (Sesti and Britt,
1992, 1993, 1994); ovariectomized, estradiol-treated
gilts (Sesti and Britt, 1992); and prepubertal gilts
(Estienne et al., 1995). Consistent with these previous findings and in the current investigation, injections of NMA reliably evoked pulses of LH and, thus,
increased the frequency of LH pulses in luteal-phase
gilts.
Increased secretion of LH following treatment of
luteal-phase gilts with NMA is most likely a consequence of NMA-induced release of GnRH from the
hypothalamus. Administration of GnRH antisera to
ovariectomized gilts abolished the ability of the
compound to increase LH secretion (Sesti and Britt,
1992), and NMA failed to alter basal or GnRHinduced gonadotropin release from rat or monkey
pituitary glands in vitro (Tal et al., 1983). Nevertheless, NMA caused increases in LH secretion from
pituitary cells collected from ovariectomized gilts and
those with intact ovaries, which suggests that the
compound may have subtle effects on the adenohypophysis (Barb et al., 1993).
In contrast to the enhanced secretion of LH
exhibited by NMA-treated luteal-phase gilts, injections of NMA had no effect on LH release in follicularphase gilts. There are at least two interpretations for
this finding. First, follicular phase gilts may be less
sensitive or completely insensitive to NMA with
regard to the compound’s ability to stimulate GnRH
and hence LH secretion. It is doubtful, however, that a
higher dose of NMA could be used to evoke LH release,
because the dosage used caused behavioral changes,
including emesis.
Alternatively, NMA might have stimulated GnRH
secretion from the hypothalamus, but there was no
corresponding increase in LH release because of
effects of estradiol on the pituitary gland. In swine,
gonadotrope responsiveness to GnRH is reduced by
estradiol prior to the emergence of the LH surge (Cox
Table 1. Mean serum concentrations (ng/mL) of GH
and cortisol in gilts before and during treatment
with n-methyl-d,l-aspartate (NMA) or
with .9% salinea
Item
Before
During
GH
NMAb
Saline
1.10 ± .06
1.03 ± .06
4.77 ± .49
1.01 ± .06
Cortisol
NMAc
Saline
54.39 ± 9.84
38.17 ± 5.53
96.43 ± 10.95
43.72 ± 8.38
aValues
bBefore
cBefore
are means ± SE.
treatment vs during treatment differ ( P < .01).
treatment vs during treatment differ ( P < .03).
ENDOCRINE RESPONSES TO N-METHYL-D,L-ASPARTATE
and Britt, 1982; Kesner et al., 1987, 1989). Following
the GnRH challenge in this experiment, concentrations of LH were lower in early follicular-phase than
in ovariectomized gilts, a finding consistent with the
notion that pituitary responsiveness was compromised
in follicular-phase animals.
The lack of an effect of NMA on LH release in
follicular-phase gilts is consistent with work by Barb
et al. (1992), who demonstrated that LH secretion in
ovariectomized, estradiol-treated gilts was unaffected
by NMA. However, using a similar model and
treatment regimen (dosages of estradiol and NMA,
timing of intramuscular estradiol injection relative to
i.v. NMA treatment, etc.), Sesti and Britt (1992)
reported that NMA increased LH secretion. Perhaps
undetermined genetic or environmental factors affect
the ability of NMA to stimulate LH secretion.
Consonant with previous reports (Barb et al., 1992;
Chang et al., 1993; Popwell et al., 1996), in the
current study, treatment with NMA decreased mean
concentrations of LH and the frequency of LH pulses
in ovariectomized gilts. Thus, in the absence of
gonadal steroids, NMA suppresses gonadotropin secretion, which raises the possibility that in addition to
their well-documented stimulatory effects, under appropriate conditions, excitatory amino acids may also
suppress gonadotropin release.
The reports by Barb et al. (1992) and Chang et al.
(1993) that NMA also suppressed LH release in
ovariectomized, progesterone-treated gilts seem incompatible with the current data, which revealed a
stimulatory effect of NMA on LH release in lutealphase gilts. It should be noted, however, that in those
previous studies (Barb et al., 1992; Chang et al.,
1993) the steroid treatment regimen used was only
marginally effective in suppressing gonadotropin
secretion. As a consequence, it may not be surprising
that when there was a high level of gonadotropin
secretion before treatment, NMA injections ultimately
resulted in a decrease in LH release.
Previous investigations demonstrated that administration of NMA increased circulating concentrations of
GH in ovariectomized gilts with or without steroid
replacement therapy (Barb et al., 1992; Chang et al.,
1993), in prepubertal gilts (Estienne et al., 1995),
and in barrows (Estienne et al., 1996). Similarly, in
the current experiment, GH secretion was evoked by
NMA in ovariectomized, luteal-phase, and follicularphase gilts.
The increase in GH secretion caused by NMA
probably involves NMDA receptors and the hypothalamic secretion of GRF. The pretreatment of barrows
with ketamine hydrochloride, an NMDA receptor
antagonist, attenuated the ability of NMA to increase
GH secretion (Estienne et al., 1996). Immunoneutralization of GRF in gilts (Barb et al., 1996)
or barrows (Estienne et al., 1996) abolished NMAinduced GH secretion. However, Barb et al. (1993)
2167
reported that NMA stimulated GH release from
pituitary cells collected from ovariectomized gilts and
gilts in the luteal phase of the estrous cycle, but not
from pituitary cells obtained from gilts in the follicular
phase of the estrous cycle.
Similar to previous studies conducted with ovariectomized gilts; ovariectomized, steroid-treated gilts;
and barrows (Barb et al., 1992; Chang et al., 1993;
Popwell et al., 1996), in the present study, NMA
increased serum concentrations of cortisol in ovariectomized, luteal phase, and follicular phase gilts. The
mechanism by which NMA increases cortisol secretion
in swine has not been ascertained. However, it is
likely that NMA stimulates secretion of corticotropinreleasing factor (CRF), which triggers pituitary
release of ACTH and ultimately cortisol secretion. In
rats, NMDA induced an increase in ACTH secretion
(Farah et al., 1991). Moreover, Reyes et al. (1990)
observed that intracerebroventricular infusion of CRF
antiserum prevented NMA-induced cortisol secretion
in ovariectomized rhesus monkeys.
In summary, NMA had profound effects on circulating concentrations of LH, GH, and cortisol in swine.
The role of excitatory amino acids in the physiological
control of hormone secretion and in the neural
mechanisms controlling growth, and reproductive
events, such as the onset of puberty and the onset of
estrus following weaning, warrants scrutiny.
Implications
Luteinizing hormone ( L H ) secretion is critical for
reproductive events such as the onset of puberty and
of estrus following weaning. Moreover, growth hormone ( G H ) stimulates growth and muscle accretion.
Under appropriate conditions in the current study, nmethyl-d,l-aspartate stimulated LH, GH, and cortisol
secretion in gilts. N-Methyl-d,l-aspartate mimics the
actions of glutamate, an important neurotransmitter
in the central nervous system. Thus, glutamate may
have an important role in the control of hormone
secretion in swine. This study provides basic information that will assist with the development of methods
to accelerate growth and enhance reproduction in
female swine.
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