USE OF GONADOTROPIN-RELEASING HORMONE

FOR HASTENING OVULATION

IN TRANSITIONAL MARES
L. A. Hanison, E. L. Squires2, T. M. Nett and A. 0. McKinnon

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Colorado State University3 Fort Collins 80523

ABSTRACT
Natural GnRH and its analog have potential for hastening ovulation in mares. A study
was conducted to evaluate the efficacy of a GnRH agonist given either as an injectable or
S.C. implant for induction of ovulation in mares. Forty-five seasonally anestrous mares
(March) were assigned to one of three groups ( n = 15/group): 1) untreated controls; 2) i.m.
injection of the GnRH agonist buserelin at 12-h intervals (40Fdinjection for 28 d or until
ovulation) and 3) GnRH agonist administered as a S.C.implant (approximately 100 ~8124h
for 28 d). Six mares per group were bled on d 0,7, 14 and 21 after injection or insertion of
implant. Samples were taken at -1, -.5 and 0 h and at .5, 1, 1.5, 2, 4, 6 and 8 h after
GnRH.Additional daily samples were drawn for 28 d after injection or until ovulation.
Samples were assayed for concentration of LH and FSH. Progesterone concentrations were
determined in samples collected on d 4, 6 and 10 after ovulation. Number and size of
follicles and detection of ovulation were determined by ultrasonography. Number of mares
induced to ovulate within 30 d was 0 of 15, 7 of 15 and 9 of 15 for groups 1, 2 and 3,
respectively. During treatment, follicle sizes were smaller for mares in group 3 (implant).
The LH response to GnRH agonist (area under c w e ) was similar among groups at d 0 but
was greater (P e .05) for mares in group 3 on d 7 and 14 and groups 2 and 3 on d 21 than
for controls. A similar pattern was detected for peak concentrations of LH after GnRH on d
0. 7, 14 and 21. Daily concentrations of LH remained low in untreated control mares
compared with GnRH-treated mares throughout the sampling period. Concentrations of LH
for mares in group 3 that ovulated were elevated greatly above those for group 2 mares,
whereas concentrations of FSH were similar in both treatment groups prior to ovulation.
(Key Words: GnRH, Ovulation, Seasonal Behavior.)
J. h i m . Sci. 1990. 68:690-699

in the hypothalamus with subsequent increased

lntmductlon
The mare is a seasonal breeder with estrous
cycles occurring during May to October
(Ginther, 1979). Transition into the breeding
season b r n winter anestrus (transitional
mares) is characterized by restoration of GnRH
'Funded in part by Colorado State Univ. Exp. Sta and
Hoechst-Rousscl Agri-Vet. Sommuville,NJ.
2~epri.trequests: E. L. squires, Equine Sciences ~ 0
gram.
3Anim. Reprod. Lab.
Rcceivcd March 7.1989.
Accepted June 27,1989.
690
synthesis and secretion of LH (Silvia et al.,
1987).
Extended photoperiod hastens cyclicity in
mares (Loy. 1968; Kooistra and Ginther,
1975). but it is necessary to initiate this
regimen 2 to 3 mo in advance of the desired
first ovulation. Investigators using progestins
(Squires et al, 1979. 1983), prostaglandin
(Lamond et al., 1975) and pituitary extract
(Douglas et al., 1974) have had limited success
in hastening ovulation. However, natural
-GnRH and its analogs have potential to hasten
ovulation in transitional mares (Johnson, 1986,
1987; Affleck et al.. 1987; Allen et al., 1987;
Fiagerald et al., 1987; Hyland et al., 1987).
 GnRH IN TRANSITIONAL MARES
Although initial studies with daily injections of
GnRH in acyclic winter anestrous mares were
of limited success (Evans and Irvine, 1976,
1977), more recent studies showed that pulsa-
tile administration of GnRH will induce
ovulation in anestrous mares (Johnson, 1986,
1987; Hyland et al., 1987). GnRH agonist
administered twice per day (Affleck et al.,
1987) or as a slow-release implant (Allen et
al., 1987) appeared to hasten ovulation in
anestrous mares.
The objective of this experiment was to
evaluate the efficacy of a GnRH agonist
(buserelin) given either as an injectable or S.C.
implant for induction of ovulation in transi-
tional mares.
M.terials and Methods
General. Forty-five nonlactating, seasonally
anestrous, light horse mares were assigned
randomly to one of three groups (n = 15/
group): 1) untreated controls: 2) i.m. injection
of the GnRH agonist buserelin4 at 12-h
intervals (40 pg/injection) for 28 d or until
ovulation, whichever came first; and 3) GnRH
agonist administered as a S.C. implant designed
to release approximately 100 pg/% h for 28 d.
Total GnRH agonist in each implant was 2.9
mg. Implants were 1 to 2 mm in diameter and
10 mm in length. A small portion on the side
of the neck was clipped and scrubbed with
iodine and the implant was inserted through a
12-gauge needle. Prior to assignment, mares
had met the following criteria: 1) largest
follicle e30 mm in diameter and 2) no
evidence of a corpus luteum based on ultraso-
nography of the ovaries for at least 30 d prior
to assignment.
As mares became available, they were
assigned to one of three replicates; five mares
per treatment group per replicate. Treatment of
mares within each of the three replicates
started March 10, 11 and 12, 1987, respective-
ly. Two mares from each treatment group,
within each replicate (six mares per treatment
group), were selected randomly to be bled.
Frequent blood samples were drawn on d 0, 7,
14 and 21 after injection of insertion of
implant and the acute effects of GnRH on
blood concentrations of LH and FSH were
4Hoecbst-Rousscl Agri-Vet Co.,Sommerville, NJ.
69I
determined. In addition, daily blood samples
were drawn for 28 d after injection or insertion
of implants, or until ovulation from the same
mares to determine chronic changes in LH and
FSH prior to ovulation. All mares were bled at
d 4. 6 and 10 after ovulation to determine
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concentrations of progesterone.
All mares were teased daily throughout the
study with a teaser stallion for detection of
estrus. Each mare’s ovaries were palpated per
rectum and examined by ultrasonography
every 3 d from February 1 until detection of a
follicle 235 mm, then daily until ovulation or
regression of the largest follicle to S25 mm in
diameter. Number and size of follicles, as
determined by ultrasonography, were recorded
at each examination period.
Mares were pastured together and had ad
libitum access to alfalfa hay, water and salt.
On the day of acute blood sampling, mares
were kept in a small corral, separate from the
remaining mares, to facilitate collection of
blood.
Blood Sampling and Hormonal Assays.
Injection of GnRH analog or insertion of
implants occurred between 0600 and 0630.
Blood samples were taken at -1, -.5 and 0 h
before GnRH and at .5, 1, 1.5, 2, 4, 6 and 8 h
after GnRH. Samples prior to GnRH (baseline
samples) were not drawn after d 0 in groups 1
and 3 because group 3 mares were fitted with a
continuous slow-release implant and untreated
control mares were not administered GnRH
(group 1). Thirty milliliters were obtained at
each sampling period by venipuncture. Blood
was allowed to clot at room temperature for 1
h. Samples then were cooled to 5°C and serum
was harvested 12 to 24 h later. Samples were
assayed for concentrations of LH (Nett et al.,
1976). FSH (Nett et al., 1979) and progester-
one (Niswander, 1973) by RIA.
Statislical Analysis. Number of mares ovu-
lating within each group were compared using
chi-square analysis. LH and FSH response to
GnRH was determined by measuring total area
under the response curve for samples taken at
0 to 8 h post-GnRH injection or insemon of
implants. Concentration of hormone at each
time period from 0 to 8 h was determined and
a curve was constructed. The area in each
trapezoid at each time period was determined.
These areas then were summed to determine
total area under the curve. Peak response was
determined by the highest concentration of
hormone detected during the 8-h sampling
692 HARRISON ET AL.

period. Comparisons were made using one-
way analysis of variance (SAS, 1987). Tukey’s
HSD test (Steel and T h e , 1980) was used to
determine significant differences among
means.
Hormonal data were arranged in two ways
did not ovulate exhibited signs of esuus (mean
8.0 f 8.5, 13.7 f 8.0 d, respectively). Thirteen
of 15 untreated control mares that did not
ovulate exhibited signs of estrus (7.0 f 7.2 d)
during the 30d treatment period.
Follicular Data. At initiation of treatment,

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for analysis, either by day of treatment period size of the largest follicle and number of
or by day prior to ovulation. Differences follicles 210, 220 and 230 mm in diameter
among means at each time period were were not different (P > .05) among groups.
determined using Students T-test. For compari- Mares that were injected with GnRH agonist
son of concentrations of LH and FSH among (group 2) and did not ovulate (n = 8) had a
groups. data were grouped into three sets: 1) similar number of follicles 210, 220 and 230
all mares in each treatment group; 2) only mm throughout the observation period com-
mares in each group that ovulated; and 3) pared with controls (n = 15). In contrast, mares
mares in each group that failed to ovulate. that failed to ovulate and were administered
Comparison among groups was made for GnRH agonist as an implant (n = 6, group 3)
mean diameter of the largest follicle and for had fewer (P c .05) follicles 210 (d 8 to 22)
number of follicles 210, 220 and 230 mm and 220 (d 10 to 26) than either group 1 or 2
diameter. Within each group, mares were mares (Figure 1). Diameter of the largest
categorized as those that ovulated (responders) follicle gradually increased in group 1 mares
and those that failed to ovulate (non- from the initiation of treatment (19.0 f 6.3
responders). At each time point, means were mm) until d 28 (33.8 f 9.3 mm). However, in
compared using a one-way analysis of vari- group 2 mares that did not ovulate, the largest
ance. Differences among means were tested mean follicular size occurred on d 14 (30.6 f
using Tukey’s HSD test. 10.2 mm) then declined slightly as the
treatment period progressed (25.0 k 5.3 mm,
28 d). Diameter of the largest follicle in group
RewltS 3 mares that did not ovulate remained the same
GnRH agonist administered either as an for the entire treatment period. In general, the
injectable or as an implant hastened (P c .05) largest mean follicular diameter was less in
ovulation in transitional mares compared with group 3 mares than in group 1 and 2 mares.
nonmted control mares. Seven of 15 mares in Number of follicles 220 mm was less (P <
group 2 responded to twice-daily injection of .lo) in group 3 mares than in group 2 mares
GnRH agonist (40pghjection) and ovulated between d 8 to 18 and less (P < .05) than in
between d 10 and 25 after initiation of group 1 mares from d 14 to 24 (Figure 2). Size
treatment (mean 18.3 f 5.2 d). Similarly, of the largest follicle was similar between
mares fitted with an implant of GnRH agonist group 2 and 3 mares from d 0 to 18 of
treatment. After d 19, group 2 mares had a
(group 3) ovulated (9 of 15) between d 4 and
larger mean follicular diameter than group 3
30 (15.8 f 9.2 d). Response time and number mares, which probably was a reflection of the
of mares responding to administration of mean ovulation date (18.3 f 5.2, group 2; 15.8
GnRH agonist were not different (P > .05) f 9.2 d, group 3).
between treated groups. Fewer (P e .05) Acute Changes in Gonadotropins. Acute
control mares (0 of 15) ovulated within 30 d of LH response to GnRH agonist (area under the
initiation of treatment than treated mares ( 16 curve) was greater (Pe .05) for mares in group
of 30). There was no difference (P > .05) in 3 than for controls on d 7, 14 and 21 (Table 1).
the number of follicles ovulated (1.3 f .5 vs The response for mares in group 2 was similar
1.1 f .3 follicles) or the size of the ovulatory (P e .05) to that for mares in both groups 1
follicle prior to ovulation (44.3 f 5.4 vs 39.4 f and 3 on d 7 and 14 but was greater (P < .05)
6.4 mm) between groups 2 and 3. than that for control mares at d 21.
Duration of estrus in mares that ovulated in Blood concentrations of FSH in response to
groups 2 and 3 was not different (P > .05) 9.0 GnRH agonist were only different (P < .OS)
f 3.1 vs 6.6 f 3.2 d. respectively). Two mares among groups at d 0 when means for groups 2
in group 3 ovulated without exhibiting signs of and 3 were similar and values for group 3 were
behavioral estrus. Seven of eight mares in greater (P e .05) than those for controls (Table
group 2 and six of six mares in group 3 that 1).
 GnRH IN TRANSITIONAL MARES 693

Peak concentrations (highest concentration mares in group 1 (controls) and group 3

during the frequent blood collection period) of
LH after GnRH administration were higher (P
<.05) for group 3 mares than for controls on d
0, 7 and 21. Concentrations of LH in group 2
mares wexe intermediate between those of
(implant).
Peak concentrations of FSH after GnRH
agonist administration were only different (P <
.05) among groups at d 0,when concentrations
in groups 2 and 3 were higher than in group 1.

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20 A Control
T 0 Inject
0 Implant I

0 5 IO 15 20 25 3
DAY
Figure 1.Follicularchange~inmaresthatfailedtoovulate.
Control n = 15 (group l),inject n=9(group2), implant n = 6
(group 3). Anow designate difference (P< .05).
694 HARRISON ET AL.

LH response, as determined by area under than on d 0. Although LH-response was

the c w e , did not change ( P > .05) during the similar ( P > .05)at all four periods in group 3
course of the treatment period in group 1 mares,there was a trend (non-significant) for a
mares. In contrast, LH response in group 2 much larger response on d 7, 14 and 21 than
mares was greater ( P < .05) on d 7, 14 and 21 on d 0. Peak concentrations of LH remained

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0 Control
o Inject
+ Implant

------o
tl
a--

6 --

4--

I .5
E
E 1.0
0
m
A
0.5

I;
0 5 IO 15 20 25 3
DAY
Figure 2. Follicularchangesin GnRH-treated mares that ovulated compared with controls. Control n = 15 (group 1). inject
n = 7 ( p u p 2). implant n = 9 (group 3). Arrows designate period where differences occurred (P< .05).
 GnRH IN TRANSITIONAL MARES 695
TABLE 1. GONADOTROPIN RESPONSE TO GnRH AGONIST STIMULATLON

Characteristic
Ana under Peak
curve, units concentration, ng/ml
Tme o i o u o a LH FSH LH FSH

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Control (n = 6) 25.9 f 29Ab 347 f 321' 6.3 f 6.4' 58.0 f 48.9'
0 Injcct(n=6) 70.5 f 51.5 764 f23@ 13.7 f 9.0* 125.4 f 34.7d
Implant (n = 6) 118.2 f 80.7 841 f 276d 23.8 f 12.0d 137.9 f 47.0d
Control (n = 6) 23.6 f 8.3' 260.4 f 78.9 6.5 f 2.5' 49.8 f 15.9
7 Injcct(n=6) 175.8 f 9O e. 389.1 f 214.0 27.1 f 15.4d 59.0 f 40.0
ImpIant (n = 5) 456.3 f 4Q0Sd 369.0 f 370.8 65.2 f 57Sd 46.6 f 41.8
Control (n = 6) 23.1 f 19.p 267.2 f 154.7 6.4 It 5.5' 58.8 f 45.2
14 Injcct(n=4) 155.8 f 47.pd 303.2 f 126.5 25.3 f 6Sd 43.0 f 17.4
Implant (n = 2) 503.7 f 481Sd 263.0 f 59.8 78.0 f 78.9d 36.3 f 10.3
coatrol (n = 6) 24.4 f 9.1' 295.8 f 143.6 7.7 * 3.8' 40.4 f 22.1
21 Inject(n=3) 225.4 f 92.od 314.5 f 141.8 33.5 f 129 43.3 f 18.1
Implant (n = 2) 432.0 f 159.F 169.8 f 52.5 72.6 f 19.1e 22.7 f 72.6
'Lconuol= nontnxued mares,Injea = GnRH agonist at 12-h intervals, and Implant = GnRH agonist implant.
bMeanfsd.
c~~cMcans within column within time pcricd with different superscripts differ. (P< .05).

unchanged in group 1 mares throughout the
treatment period. Group 2 had greater (P <
.05)peak concentrations of LH ond 7, 14 and
21 than on d 0. Although mean peak concen-
trations of LH increased between d 0 and d 7
and 14 in group 3, this change was not
significant due to the large variation in
response at d 7 and 14.
Chronic Changes in GoMdotropins. Prior
to treatment on d 0. concentrations of LH
among groups were similar (P > .05, 1.7 f .9,
6.5 f 12.1 and 6.5 f 6.5 ng/ml, respectively,
for groups 1. 2 and 3). Mares in group 1 had
minor elevations in plasma concentrations of
LH during the treatment period with a differ-
ence (P < .05)only between d 0 and d 28 (1.7
f .9 vs 6.3 f 2.6 ng/ml). Mean concentrations
of FSH in these mares fluctuated between 25.7
f 8.1 ng/ml and 56.8 ng/ml during the
treatment period (Figure 3).
Changes in FSH and LH concentrations for
group 2 and 3 mares that did not ovulate were
similar (P > .05;Figures 3a and 4a). In both
GnFtH-treated groups, concentrations of LH
increased from d 0 to 7 and then remained
relatively constant from d 7 to 28, except for
randomly elevated concentrations detected in
group 2 mares (Figure 4a). Concentrations of
LH in both treated groups were greater (P <
.OS) than those in control mares throughout the
treatment period. Concentrations of FSH in
control mares and GnRH-injected mares were
similar throughout the sampling period,
whereas FSH concentrations in GnRH-im-
planted mares tended to be suppressed after d
7 compared with the other two groups (Figure
3a).
Mares in group 3 that ovulated had in-
creased concentrations of LH from d -23 until
d -15 (Figure 4b). Thereafter, concentrations
of LH decreased between d -15 and -10, then
increased to a second smaller peak at d -5. A
similar profile of LH was not detected in
GnRH-injected mares.
Concentrations of FSH in GnRH-treated
mares that ovulated decreased toward the latter
part of the treatment period (Figure 3a). The
changes in concentrations of FSH were similar
between the two GnRH treatment groups.
Mean concentrations of LH on the day of
ovulation were similar (P > .OS) in group 2
and 3 mares (12.1 f 3.8 ng/ml vs 47.4 f 40.0
ng/ml). Concentrations of FSH also were
similar for group 2 and 3 mares on the day of
ovulation (21.7 f 3.8 vs 24.8 f 14.1 ngfml).
Progesterone concentrations on d 4, 6 and
10 post-ovulation were not different (P > .OS)
between group 2 and 3 mares, although group
3 mares tended to have slightly higher
concentrations at each respective time period.
Discussion
Turner et al. (1979) characterized patterns
of follicular development and serum concentra-
6% HARRISON ET AL.

tions of gonadotropins during anestrus and another study (Hart et al., 1984), pituitary
transition into the breeding season.About 60 d concentrations of FSH did not vary throughout
prior to the first ovulation, the number of large the year, but concentrations of LH were
follicles (>20mm) increased and number of dramatically lower in December and March
small follicles decreased. Nine days prior to than in July and October. Silvia et al. (1987)
ovulation, there was a rapid increase in administered single injections of GnRH during

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diameter of the largest follicle and concentra- anestrus, early transition and late transition and
tions of LH in serum. Freedman et al. (1979) demonstrated that the LH response increased,
reported a significant decline in concentrations whereas the FSH response decreased, from
of FSH beginning 20 d prior to ovulation. In anestrus to the breeding season. They attrib-

loo- 0Control
A Inject
80-- + Implant
-
h

\
E 60-
0

-I
c
40-
v,
20-

0 1
1 1
1
I
1
I
1
I I I

80-
A Inject
70- 0 Implant
=E 60--
50-
-0
c
40-
5 30--
20-
IO--
04 1 I 1

-25 -20 -15 -10 -5 0

DAY
Figure 3. Changes in concentrationsof FSH in mares that failed to ovulak (a) -control n = 6 (goup 1). inject n = 1 (group
Z), implant n = 1 (group 3) - md changes in concentrations of FSH relative to ovulation (b). Inject n = 5, implant n = 5.
 GnRH IN TRANSITIONAL MARES 697

uted this to increased pituitary stores of LH. istration of GnRH agonist in implant form
The increased response to GnRH agonist over resulted in a greater response area under the
time in the present study indicated that GnRH curve, peak concentrations and daily serum
agonist increased pituitary stores of LH by d 7 concentrations of LH and a more rapid and
in mares given the implant and by d 21 for larger decline in FSH response parameters than
mares injected with GnRH agonist. The de.- twicedaily administration.
creased FSH response during the 1st wk of The reason(s) for some mares’ failure to

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GnRH agonist treatment also was analogous to ovulate in the GnRH-treatment groups was not
the diminished response in late transitional determined. However, two possible causes are
mares reported by Silvia et al. (1987). Admin- an insufficient concentrations of FSH to

50T 0 Control
A Inject
f + Implant

c 1 I
I
1 I
I
1 I I I

-4 0 4 8 12 16 20 24 28 32
DAY

A nject
IlO+ 0 mplant
90-
h

-
E 70-
\
50-
v

I 30-
A
10-

I I
I

-25 -20 -15 -10 -5 0

DAY
Figure 4. Chronic changesin concentrationsof LH in mares that failed to ovulate (a) -control n = 6 (group l), inject n = 1
(group2), implatll n = 1 (group 3) - and concentrationsof LH relative to ovulation (b). Inject n = 5 , implant n = 5.
698 HARRISON ET AL.
stimulate follicular growth and down-regula-
tion of LH receptors at the ovarian level. Only
one group 3 mare that was bled did not
ovulate. Her serum concentrations of FSH
were only slightly lower than those of group 1
and 2 mares that did not ovulate. Therefore,
from these data it is impossible to determine
whether failure to ovulate was a consequence
of low FSH levels. Amundson and Wheaton
(1979) demonstrated a significant reduction in
the number of ovarian follicles greater than 2
mm in diameter when ewes were given
continuous LHRH for 4 wk. In their experi-
ment, concentrations of LH in LHRH-treated
sheep were within the range of control levels
but did not fluctuate to the same degree as they
did in control ewes. Therefore, it was hypothe-
sized that periodic pulses of circulating LH are
necessary for follicular growth. In light of data
from the present study whereby LH showed
minimal fluctuation during the frequent sam-
pling period and follicular populations were
significantly reduced in group 3, this hypothe-
sis may be applicable. However, in addition to
the absence of periodic fluctuations in LH
concentrations in group 3, mean LH concenua-
tions were greater than in either group 1 and 2
mares.
Hyland et al. (1987) found that mares
responding to GnRH had biphasic LH profiles
with peaks at approximately d 6 and 16 to 20
after initiation of treatment, with ovulations
occurring near the second peak. Mares that
failed to ovulate exhibited the first peak, but
then LH concentrations declined toward base-
line. In the present study, mares in group 3 that
ovulated demonstrated a biphasic profile simi-
lar to that reported by Hyland et al. (1987),
with peaks near -5 and -15 d prior to
ovulation (Figure 4b). Failure of mares to
ovulate that were treated with pulsatile GnRH
(group 2) did not appear to be due to
suppression of follicular activity, but rather to
a failure to cause, directly or indirectly, a
sufficient decline in FSH concentrations
and(or) a sufficient increase in concentrations
of LH to result in a reciprocal relationship
between these two gonadotropins. This recip
rocal relationship has been indicative of an
ensuing ovulation in both transitional (Freed-
man et al., 1979) and postpartum (Hines et al.,
1987) mares. The 100 pgld dose as a
continuous implant may have been too high
and resulted in suppression of ovarian activity,
and the 40 pg dosage given and 12-h intervals
was too low to be consistently effective. This
is supported by data from experiments using
lutrelin, which consistently induced ovulation
in early and late transitional mares (Affleck et
al., 1987; Fitzgerald et al., 1987) when
administered at the rate of 100 pg every 12 h.
Comparisons between concentrations of
gonadopropins in ovulating and non-ovulating
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mares did not indicate a pattern that would
allow one to predict which mares would
respond to GnRH administrations and ovulate.
Implications
A GnRH agonist hastened the initial ovula-
tion of the breeding season in mares. The
ability to administer GnRH agonist via a
subcutaneous implant has practical applica-
tions for early foal production. Although these
results are encouraging, further studies are
needed to determine the most effective dose of
GnRH agonist for hastening ovulation in
anestrous mares.
Literature Cited
Affleck, K.J.. R. G. Loy and B. P. Fitzgerald. 1987. Serum
gonadotropin concentrations in mares treated with a
GnRH agonist to induce ovulation. Proc. 19th Equine
Nuu. and Physiol. Symp. p 325.
Allen, W. R., M. W. Sanderson, R.E.S. Greenwood. D. R.
Ellis, J. S. Crowhurst, D. J. Simpson and P. D.
Rossdale. 1987. Induction of ovulation in anestrous
mares with a slow-release implant of a GnRH analogue
(IC1 118 630). 1. Reprod. Fertil. Suppl. 35:469.
Amundson, B. C. and J. E. Wheaton. 1979. Effects of
chronic LHRH treaunent on brain LHRH and ovarian
follicular activity in the anestrous ewe. Biol. Reprod.
20:633.
Douglas,R. H., L.Nuti and 0.J. Ginther. 1974. lnduction of
ovulation and multiple ovulation in seasonally-anovu-
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genology 2:133.
Evans, M. J. and C.H.G. Irvine. 1976. Measurement of
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hormone: Response of anestrous mares lo gonadotro-
pin releasing hormone. Biol. Reprod. 15:477.
Evans, M.J. and C.H.G. Irvine. 1977. lnduction of follicular
development. maturation and ovulation by gonadotro-
pin releasing hormone administration to acyclic mares.
Biol. Reprod. 16:452.
Fitzgerald. B. P..K. J. Affleck, R. Pemstein and R. G . Loy.
1987. Investigation of the potential of LHRH or an
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