Recent experimental observations have shown that the thyroid gland pla
ys a dominant part in the induction and maintenance of anoestrus in ew
es. The mechanisms of the anoestrous effects of the thyroid gland are
still unclear. On the basis of experiments, in which after thyroidecto
my at the onset of sexual activity LH production was maintained also d
uring the spring months, iodothyronines have been supposed to stimulat
e the inhibitory effects of oestrogens upon the neuroendocrine centres
that generate pulsatile LH secretion (Moenter et al., 1991; Webster e
t al., 1991). However, in our previous work (Bekeova al., 1995) we obs
erved significant changes in iodothyronine levels, mainly T-3, in ewes
treated with FSH, LH-RH and oxytocin-based preparations in 24 and 72
h after parturition in the spring. Having made the above observations
we suppose seasonal anoestrus to result rather from changes in thyroid
and ovarian hormone interactions or from a decrease in thyroid hormon
e levels that is induced by a temporary decrease in sexual hormones in
this phase of the year. Within investigations into the effects of thy
roid hormones and their interactions in spring this study focused on t
he response of the thyroid gland and ovaries in anoestrous ewes to chl
orsuperlutin and PMSG treatment in the second half of May. Eighteen Sl
ovak Merino ewes were divided into an experimental and a control group
counting 15 and 3 animals, respectively. The experimental animals wer
e each treated with 20 mg chlorsuperlutin (Agelin Spofa vaginal insert
s) for 12 days. On day 12 the inserts were removed and each animal was
given 500 IU PMSG. In the same time intervals the controls were treat
ed with a placebo (sterile polyurethane, saline). Blood samples were o
btained prior to swab insertion (day 0) and in 4-day intervals under c
hlorsuperlutin treatment (days 4, 8 and 12). For the First 24 h after
PMSG-treatment blood samples were taken in 2-hour intervals and then i
n 48 and 72 h. For radioimmunological determination of T-4, T-3, E(2)
and P-4 levels the RIA-test-T-4, RIA-test-T-3, RIA-test-Estra and RlA-
test-Prog commercial kits (manufacturer: URVJT Kosice Slovak Republic)
were used, respectively. When compared to the almost constant but sig
nificantly lower T-4 values in the controls (P < 0.05; P < 0.01; Tab.
II, Fig. 1), a repeated massive release of T-4 occurred in the experim
ental animals (Tab. I, Fig. 1). Its first peak observed 4 h after PMSG
was significant in comparison both to Day 0 and the controls (P < 0.0
5 and P < 0.01, respectively). The same was true for the 2nd peak obse
rved 20 h after PMSG-treatment (P < 0.001 and P < 0.01, respectively).
The dynamics of T-3 was similar in both groups. The transitory increa
se in .T-3 levels observed in the controls (Tab. II, Fig. 2) on day 4
of chlorsuperlutin treatment was insignificant when compared to day 0.
Both the decrease observed between day 8 of chlorsuperlutin treatment
and 20 h after PMSG gavage, and the increase between 24 and 72 h appe
ared to be insignificant. Comparison to day 0 revealed increased T-3 l
evels in the experimental group (Tab. I, Fig. 2) on days 4 and 8 of ch
lorsuperlutin treatment, the levels of significance being P < 0.01 and
0.05, respectively. Between 8 and 24 h after PMSG-gavage, in contrast
to the controls, T-3 levels in the experimental animals acquired the
character of a slowly increasing rhythmic pulsation. At 72 h after PMS
G a significant decrease occurred (P < 0.05). In the control animals (
Tab. II, Fig. 3) E(2) levels revealed interchanging episodes of insign
ificant increase and decrease beneath lest sensitivity. In the experim
ental ewes (Tab. I, Fig. 3) a double-peaked elevation of E(2) could be
observed, the first (insignificant) peak occurring 18 and 20 h and th
e second (significant) one 48 and 72 h following PMSG treatment (P < 0
.05 and 0.01, respectively). The inter-group differences were signific
ant at the level of P < 0.05 in each case. P-4 levels in the controls
(Tab. II, Fig. 4) ranged within 1.2 and 3.4 nmol/l serum, except of a
decrease in 10 and 48 h that was insignificant when compared to day 0.
In the experimental ewes (Tab. I, Fig. 4) Pq levels revealed a gradua
l decrease, reaching their lowest values (significant in comparison to
Day 0 at the level of P < 0.001) between 22 and 24 h after PMSG treat
ment. Comparison to the controls revealed the lowest P between 12 and
20 h after PMSG-treatment (P < 0.05, P < 0.01; P < 0.001): The changes
in both iodothyronine levels that could be observed after chlorsuperl
utin and PMSG treatment were partly different from those published by
Moenter et al. (1991) and Webster et al. (1991). In agreement with the
above authors we suppose the changes in thyroid and ovarian hormone i
nteractions to be the cause of seasonal anoestrus induction and mainte
nance. On the basis of the obtained results we suppose that the depres
sion of the secretion of iodothyronines is the basic mechanism respons
ible for the onset of the seasonal anoestrus as well as for its durati
on. We suppose that the changes in the secretion of sexual hormones as
well as their controlling elements in spring are responsible for the
decreased activity of the thyroid gland.