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JEZ 818
126
A.C. HOLLOWAY
THE JOURNAL
AND J.F. OF
LEATHERLAND
EXPERIMENTAL ZOOLOGY 279:126–132 (1997)
Effects of N-Methyl-D,L-Aspartate (NMA) on
Growth Hormone and Thyroid Hormone Levels
in Steroid-Primed Immature Rainbow Trout
(Oncorhynchus mykiss)
ALISON C. HOLLOWAY1 AND JOHN F. LEATHERLAND2*
1
Department of Zoology, University of Guelph, Guelph, ON N1G 2W1,
Canada
2
Department of Biomedical Sciences, University of Guelph, Guelph,
ON N1G 2W1, Canada
ABSTRACT
In this study we investigate whether the stimulatory action of the glutamate
agonist, N-methyl-D,L-aspartate (NMA) on growth hormone (GH) levels in rainbow trout (Oncorhynchus mykiss) is steroid hormone-dependent. NMA was administered to sexually immature
juvenile rainbow trout that had been primed with testosterone (T), 17β-estradiol (E2) or 5αdihydrotestosterone and changes in plasma growth hormone (GH) concentrations were measured.
NMA had no significant effect on the plasma GH concentrations of non-steroid hormone-primed
trout (controls), although in both T- and E2-primed fish plasma GH levels were elevated 6 hours
following NMA administration. The response had disappeared by 24 hours in the T-primed group,
but was still evident in the E2-primed fish. In comparison, in the 5αDHT-primed fish, NMA significantly depressed plasma GH levels 6 hours post-injection (P < 0.05), but this effect had disappeared 24 hours after NMA administration.
NMA had no effect on plasma T4 levels in any treatment group, and although plasma T3 levels
were significantly (P < 0.05) depressed in T-primed fish 6 hours post-injection, this response was
not seen in any other group. These results suggest that NMA has no effect on plasma thyroid
hormone levels but it does have a steroid hormone-dependent action on plasma GH levels in rainbow trout. J. Exp. Zool. 279:126–132, 1997. © 1997 Wiley-Liss, Inc.
Several different lines of investigation have provided evidence to suggest that growth hormone (GH)
plays a key role in the reproductive physiology of
teleost fishes (Le Gac et al., ’93). First, extremely
high levels of GH have been found in sexually mature white sucker, Catostomus commersoni (Stacey
et al., ’84), rainbow trout, Oncorhynchus mykiss
(Sumpter et al., ’91), goldfish, Carassius auratus
(Trudeau et al., ’92), coho salmon, Oncorhynchus
kisutch (Flett and Leatherland, unpublished data),
Atlantic salmon, Salmo salar (Björnsson et al., ‘94),
and chum salmon, Oncorhynchus keta (Kakizawa
et al., ’95). Second, the administration of gonadal
steroid hormones has been shown to increase
plasma GH levels in vivo in hybrid tilapia,
Oreochromis niloticus × O. aureus (Melamed et
al., ‘95b), goldfish (Trudeau et al., ’92), carp,
Cyprinus carpio (Lin et al., ’95), and rainbow trout
(Holloway and Leatherland, ‘97a). Third, the administration of exogenous GH appears to stimulate gonadal steroid production in several species
of fishes (Le Gac et al., ’93). In addition, several
© 1997 WILEY-LISS, INC.
factors that are known to influence the activity of
the hypothalamic-pituitary-gonadal axis, including gonadotropin-releasing hormone (GnRH),
dopamine (DA), neuropeptide Y, and the glutamate
analogue, N-methyl-D,L-aspartate (NMA), are also
known to affect GH release (Marchant et al., ’89;
Chang et al., ’90; Peng et al., ’90; Lin et al., ’93;
Flett et al., ’94; Lin et al., ’95; Trudeau et al., ’90).
NMA, which is generally considered to be specific for the NMDA-type glutamate receptor, has
been shown to stimulate both GH and luteinizing
hormone (LH) secretion in vivo in a range of mammalian species (rat, mouse, sheep, pig, monkey
(Gay and Plant, ’87; Acs et al., ’90; Barb et al.,
’93; Brann and Mahesh, ’92; l’Anson et al., ’93;
Miller and Gibson, ’94; Akema et al., ’95; Pinilla
Contract grant sponsors: NSERC, OMAFRA, and DFO.
*Correspondence to: Dr. John Leatherland, Department of Biomedical Sciences, Ontario, Veterinary College, University of Guelph, Guelph,
ON N1G 2W1, Canada. E-mail: jleatherland@ovcnet.uoguelph.ca
Received 23 September 1996; Revision accepted 7 April 1997.
EFFECT OF NMA ON GH RELEASE IN RAINBOW TROUT
et al., ’95; Downing et al., ’96; Estienne et al., ’96).
In rainbow trout, NMA was found to have a similar stimulatory effect on in vivo plasma GH and
gonadotropin (GtH) levels following testosterone
(T)-priming of juvenile animals (Flett et al., ’94).
In contrast, Trudeau et al. (’96) describe an inhibitory effect of NMA on GH release in goldfish,
although the levels of NMA which elicited a response in that study (25 and 50 µg g-1 body weight)
were considerably higher than those used in either the Flett et al. (’94) study or the one described
here (1 µg g-1 body weight).
Recent studies in mammals suggest that NMA
elevates GH indirectly via the increased release
of GH releasing hormone (GHRH) (Acs et al., ’90;
Barb et al., ’96; Estienne et al., ’96). In addition,
a direct action of NMA on the pituitary cells in
vitro was also reported for rat (Lindström and
Ohlsson, ’92; Niimi et al., ’94) and pig (Barb et
al., ’93) pituitary cells cultured in vitro. Furthermore, the NMDA R1 receptor subunit has been
co-localized with GH cells in the rat anterior pituitary (Bhat et al., ’95). Conversely, several other
studies have failed to find a GH-stimulatory action of NMA (Acs et al., ’90; Barb et al., ’93;
Cocilovo et al., ’92; Liaw and Barraclough, ’93).
In addition to its effects on GH release, NMA
stimulates both the synthesis and release of hypothalamic GnRH in mammals (Brann, ’95). Similarly, in vitro studies in rainbow trout show that
the gonadotropic cell response to both NMA and
GnRH is completely abolished in the presence of
a GnRH antagonist (Flett et al., ’94). These results suggest that the stimulatory action of NMA
on GnRH release in rainbow trout is similar to
that seen in mammalian models. Since GnRH is
both a potent GtH- and GH-releasing factor in several fish species (Marchant et al., ’89; Marchant
and Peter, ’89; Chang and De Leeuw, ’90; Lin et
al., 93; Lin et al., ’95; Melamed et al., ‘95a), it is
possible that the GH-stimulatory action of NMA
in rainbow trout is mediated by GnRH.
The ability of NMA to stimulate LH release in
mammals is enhanced in the presence of gonadal
steroid hormones (Brann and Mahesh, ’92; Arias
et al., ’93; Brann, ’95), probably via an increased
responsiveness of the LH cells to LHRH (Arias et
al., ’93). Similarly, the GH response to NMA is
also enhanced by gonadal steroid hormones. For
example, Barb et al. (’93) reported that NMA
stimulated GH release from isolated pituitary cells
taken from either ovariectomized pigs, or pigs in
the luteal phase of the estrous cycle, but did not
stimulate GH release from pituitary cells taken
127
from pigs during the follicular phase of the estrous cycle. Similarly, Chang et al. (’93) found that
progesterone potentiated the GH response to NMA
in ovariedomized pigs. There is only limited information about the effects of NMA on GH release
in teleost fishes, but preliminary reports suggest
that the action of NMA, at least in trout and goldfish, is modulated by gonadal steroid hormones
(Flett et al., ’94; Trudeau et al., ’96).
The main purpose of the study reported here
was to examine the effects of NMA on plasma GH
concentrations in juvenile rainbow trout, and to
evaluate whether the secretion of GH in response
to NMA challenge is influenced by the presence
of sex steroid hormones. A second component of
the study was to evaluate whether NMA influences thyrotropic cell function; for this part of the
study, plasma thyroxine (T4) concentrations were
measured as an indication of the possible effects
of NMA on thyroid hormone secretion. This aspect of the study was undertaken because in mammals, one of the known NMA receptors (the NMDA
R1 receptor subunit), in addition to being present
in the GH cells, is also found in the TSH cells
(Bhat et al., ’95). The co-localization of the NMDA
R1 receptor subunit with GH and TSH cells might
be indicative of a role of NMA in the regulation of
the hypothalamic-pituitary-thyroidal axis.
MATERIALS AND METHODS
Two hundred juvenile (sexually immature) rainbow trout (Oncorhynchus mykiss) were used in the
study. The fish were held in fibreglass tanks supplied with constantly running aerated well water
at 9 ± 2°C under a simulated natural photoperiod
for 2 months prior to the experiments. They were
fed to satiety daily with commercial pelleted trout
food (Martin’s Feed Mills, Elmira, Ontario) for the
duration of the experiment.
Two separate trials were undertaken, the first
employing 160 trout of approximately 105 g body
weight and the second employing 40 trout of approximately 200 g body weight. At the commencement of each trial of the study, the fish were
anaesthetized in MS222 (25 mg 1-1) and given a
slow release implant of steroid hormone (7.5 µg
g-1 body weight) dissolved in approximately 0.3 ml
of warm hydrogenated coconut oil or coconut oil
alone (control). Steroid hormone implants at this
level have been shown to significantly elevate
plasma steroid hormone levels for up to 8 weeks
post-implantation (Flett and Leatherland, ’89).
In the first trial, groups of trout were administered coconut oil alone or oil containing testoster-
128
A.C. HOLLOWAY AND J.F. LEATHERLAND
one (T), 17β-estradiol (E2) (Sigma Chemical Co.
St Louis, MO), or the non-aromatizable androgen,
5α-dihydrotestosterone (5αDHT) (Ikapharm, Israel). In the second trial, groups were administered T or E2.
Two weeks following the steroid implantation,
each fish was given an intraperitoneal injection
of either NMA (1 µg g-1 body weight; Sigma Chemical Co. St. Louis, MO) dissolved in 100 µl of 0.8%
saline or saline alone; fish were sampled 6 and
24 hours later. (The times of sampling were chosen based on the protocol used by Flett et al. (’94)
who demonstrated an effect of NMA on plasma
GH levels within 6 hours of administering the
glutamate agonist. The dosage of NMA used was
determined in preliminary studies of the toxicity
of the compound in immature rainbow trout; 1 µg
g-1 body weight was found to elicit no obvious adverse response, whereas at 10 or 100 µg g-1 the
fish appeared to lose the ability to maintain body
posture in the water column, and at the higher dosage there was 25% mortality within 1 hour.) Each
fish was anaesthetized in MS222 (125 mg 1-1),
weighed, and bled into heparinized tubes following caudal severance; plasma was stored at
–70°C until analyzed for GH and thyroid hormone
concentrations.
Plasma GH levels were measured using a noncompetitive enzyme linked immunosorbent assay based on monoclonal antibodies developed
against salmon GH (Farbridge and Leatherland,
’91). Plasma T4 levels were measured using the
Amersham Amerlex radioimmunoassay (RIA)
(Johnson and Johnson Clinical Diagnostics,
Markham, Ontario); this RIA has been validated for use with rainbow trout plasma
(Leatherland and Farbridge, ’92). Plasma hormone levels for the NMA- and saline-treated
groups were compared within a steroid-treated
group using Student’s t-test (α = 0.05).
Fig. 1. Effect of NMA (solid bars) treatment on plasma
GH levels in immature steroid primed rainbow trout. Data
are shown as ng ml-1 GH (mean ± SEM), n = 10 for each
group. *Significantly different from their respective saline
(open bars) controls (P < 0.05).
RESULTS
NMA had no significant effect on plasma GH
levels in the oil primed group at either 6 or 24
hours post-injection (Fig. 1). However, in the
groups that had been given an implant containing either E2 or T, plasma GH levels were significantly elevated at 6 hours post-injection. In the
T-primed group this response was not evident 24
hours post-injection, but in the E2 primed fish,
plasma GH levels were still elevated with respect
to the saline control group 24 hours after the administration of NMA. The stimulatory effect of
NMA on T- and E2-primed trout was confirmed in
a second trial; in both groups, plasma GH levels
of the NMA treated animals were significantly elevated 6 hours post-injection (testosterone-primed:
saline 3.71 ± 0.34 ng ml-1, NMA 6.50 ± 1.16 ng
ml-1 (P < 0.05); estradiol-primed: saline 2.42 ± 0.59
ng ml-1, NMA 4.84 ± 0.82 ng ml-1 (P < 0.05)).
In the group of fish administered 5αDHT, a nonaromatizable androgen, NMA acted to significantly depress plasma GH levels 6 hours after its
administration, although this response was not
evident after 24 hours (Fig. 1).
EFFECT OF NMA ON GH RELEASE IN RAINBOW TROUT
NMA treatment had no effect on plasma T4 levels in any group either 6 or 24 hours post-injection (Table 1).
DISCUSSION
In this study, in immature trout that had been
primed with either T or E2, followed 2 weeks later
by an NMA challenge, there was an increase in
plasma GH concentrations 6 hours following the
injection of NMA; the response was particularly
marked in the E2-primed group. The GH stimulating action of NMA was not seen in trout that
had been given only an oil implant. Moreover, in
the group of trout that had been primed with the
non-aromatizable androgen, 5αDHT, NMA elicited
a significant decrease in plasma GH concentrations. Thus, the response to NMA is clearly dependent on the nature of the steroid milieu, and
the permissive effect of steroid hormones on a
plasma GH increase apprears to be related to the
presence of either an estrogen or an aromatizable
androgen.
These findings confirm an earlier study in which
T-primed immature rainbow trout exhibited a significantly elevated plasma GH concentration 6
hours following an intraperitoneal injection of
NMA (Flett et al., ’94). However, the findings are
contrary to those of Trudeau et al. (’96) in which
NMA was administered to steroid hormone-primed
goldfish. Those authors found that NMA, administered intraperitoneally, acted to inhibit the
stimulatory action of E2 on plasma GH concentrations. The differences in the two studies
might reflect species differences, although they
are more likely linked to the NMA levels that
were applied in the two studies. In the goldfish
study, the NMA levels that elicited a significant
GH response were 25 and 50 µg g-1 body weight
and 50 µg per fish for intraperitoneal and intraventricular administrations, respectively,
129
compared with only 1 µg g-1 body weight for the
Flett et al. (’94) study and the one reported
here. In our laboratory, intraperitoneal doses
10 µg g-1 and higher were neurotoxic, as evidenced by abnormal swimming behaviour and
apparently impaired balance.
The means by which NMA affects GH secretion
in fishes has yet to be established. In mammals,
the glutamate agonist may act via the NMDA receptor, to stimulate somatostatin (SRIF) secretion
and synthesis in vivo and in vitro (Rage et al.,
’94). Paradoxically, SRIF has been identified as a
potent GH-inhibitory factor in teleost fishes (Peter and Marchant, ’95); therefore, a NMA-stimulated increase in SRIF release would lower plasma
GH concentrations and is inconsistent with the
results of the study presented here for the E2- and
T-primed trout, but may explain the inhibitory action of NMA in the 5αDHT-primed fish. Conversely, in mammals there is also evidence to
suggest that the GH-stimulatory action of NMA
is mediated via an increase in the release of GHreleasing hormone (GHRH) from the hypothalamus (Acs et al., ’90; Barb et al., ’96; Estienne et
al., ’96). Heterologous GHRH has been shown to
increase GH release from isolated rainbow trout
pituitary cells (Luo et al., ’90; Blaise et al., ’95),
and the possibility that NMA stimulates GH release indirectly through increased hypothalamic
GHRH release cannot be refuted. However, only
few GHRH fibres are found to innervate the pars
distalis in teleost fishes (Rao et al., ’96) and
Marchant and Peter (’89) were unable to find a
GHRH-stimulated GH release from perifused goldfish pituitary glands, suggesting that GHRH may
not be an important physiological regulator of GH
secretion in teleosts. On the other hand, Flett et
al. (’94) showed that NMA had a potent stimulatory effect on GtH release from perifused pituitary
glands of T-primed rainbow trout, which would
TABLE 1. Effect of NMA treatment on plasma T3 and T4 concentrations in rainbow trout1
Time after
NMA injection
6 Hours
24 Hours
1
T3 (nmol l–1)
Implant
Oil
E2
T
5αDHT
Oil
E2
T
5αDHT
Saline
3.95
10.71
5.23
9.54
2.88
8.76
4.51
6.24
±
±
±
±
±
±
±
±
0.86
0.57
.071
0.76
0.94
0.90
0.76
.068
Data are shown as nmol l–1 (mean ± SEM), n = 10 for each group.
*Significantly different from their respective saline controls (P < 0.05).
T4 (nmol l–1)
NMA
8.18
11.53
3.09
9.52
3.94
9.26
4.52
6.19
±
±
±
±
±
±
±
±
2.20
0.65
0.71*
0.68
0.68
0.63
0.79
0.56
Saline
14.98
6.87
9.28
8.66
6.55
6.05
7.90
6.08
±
±
±
±
±
±
±
±
3.25
0.31
0.88
1.10
1.17
0.44
1.37
1.17
NMA
19.02
7.20
9.91
9.75
8.12
5.86
10.69
7.34
±
±
±
±
±
±
±
±
2.40
0.74
2.23
0.91
0.83
0.46
2.23
0.80
130
A.C. HOLLOWAY AND J.F. LEATHERLAND
suggest that, as in mammals, NMA increases the
release of GnRH. Since GnRH has been shown to
have a potent GH-stimulatory effect in several teleost fishes (see Introduction for references),
mostly cyprinid species, it is possible that NMA
affects GH release via altered GnRH release from
the hypothalamus. However, although GnRH has
been shown to stimulate GH release in rainbow
trout in vitro, the GH-stimulatory action of NMA
was not attenuated in the presence of a GnRH
antagonist (Holloway and Leatherland, ‘97b).
These data suggest that the GH-stimulatory action of NMA in rainbow trout may not be mediated via GnRH.
In mammals, NMA may affect GH release via a
direct action on pituitary cells (see Introduction
for references). Although there is no published evidence to show that NMA acts directly at the pituitary level to stimulate GH release in teleost
fishes, in vitro studies in our laboratory found that
NMA stimulates GH release from perifused rainbow trout pituitary fragments (Holloway and
Leatherland, ‘97b), suggesting that there may be
a direct action of NMA on GH release.
It is not clear how the steroid hormone milieu
can affect the GH response to NMA in rainbow
trout. In mammals, Brann et al. (‘93b) proposed
that the steroid hormone milieu might influence
the number or affinity of hypothalamic NMDA receptors; however, gonadectomy with or without
steroid hormone replacement did not change
NMDA receptor binding or NMDA receptor mRNA
levels in rats (Brann et al., ‘93b; Brann, ’95), suggesting that steroid modulation of NMA action in
mammals does not act via alterations of the hypothalamic NMDA receptors. A steroid hormone
effect on pituitary NMDA receptor levels has also
been proposed, and steroid hormone treatment
has been shown to cause changes in pituitary
NMDA receptor mRNA levels in rats (Brann el
al., ‘93a), suggesting a possible site of steroid hormone action in mammals. An alternate modus operandi is that steroids alter the sensitivity of
somatotropic cells to either NMA itself, or to the
hypothalamic factors that are released in response to NMA challenge. In support of this thesis, E2 potentiates GHRH-induced GH release
from rat anterior pituitary cells in vitro (Simard
et al., ’86), and the GnRH-induced release of GH
in goldfish and carp (Trudeau et al., ’92; Murthy
et al., ’94; Lin et al., ’95).
In the present study, there was no evidence of
an NMA effect on the hypothalamic-pituitary
gland regulation of thyroid activity. In rats, the
NMDA R1 receptor subunit has been co-localized
with approximately 6% of TSH cells in the rat
anterior pituitary (Bhat et al., ’95); no evidence
of a similar situation was found in the present
study based on measures of changes in plasma T4
levels. It is possible that the sampling times were
not appropriate to identify changes in plasma T4
concentrations in response to altered TSH release.
However, in several studies employing exogenous
TSH-challenges as measure of thyroid hormone
secretion in salmonid fishes, maximal plasma T4
concentrations were evident between 6 and 24
hours after the injection of TSH (Leatherland, ’94).
This study has shown that NMA has GH-regulatory actions in rainbow trout, although the GH
response appears to be dependent on the steroid
hormone milieu. However, there is currently no
information regarding the site of steroid modulation of NMA’s action of GH release.
ACKNOWLEDGMENTS
We thank Dr. P.K. Reddy and the staff at the
Alma Research Station for their technical assistance at several stages of the study, and Dr. H.
Kawauchi for the generous donation of recombinant salmon GH used for standards in the ELISA.
This work was supported by NSERC, OMAFRA,
and DFO grants to J.F.L., and a NSERC scholarship to A.C.H.
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