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treatment, metamorphic events were induced in a dose dependent manner,
with T3 being several times more potent than T4 (Miwa and Inui, 1987b).
de Jesus et al. (1990), using the in vitro culture of the dissected,
elongated fi n rays of prometamorphic larvae, also showed that both T4
and T3 administration to the culture medium accelerated shortening of the
fi n rays dose-dependently, with T3 being more potent than T4. The direct
effect of thyroid hormones on fi n ray resorption of the fl ounder during
metamorphosis seems comparable to the case of regression of tadpole tail
fi n discs in vitro (Derby, 1968; Robinson et al., 1977).
Induction of precocious metamorphosis by T4 administration and
metamorphic stasis by TU treatment have also been reported in summer
fl ounder, Paralichthys dentatus (Huang et al., 1998; Schreiber and Specker,
1998) and Atlantic halibut, Hippoglossus hipoglossus (Solbakken et al.,
1999).
In amphibian metamorphosis, each tissue has its own “readiness” and
the threshold level of thyroid hormone to which the tissue responds and
starts metamorphic changes (Kollros, 1961). Even in the same tissue, the
sequence of the metamorphic changes sometimes requires different levels
of thyroid hormone (Kollros, 1961). For the fl ounder, TU-treated larvae still
initiated eye migration but did not complete it, while fi n ray shortening
was completely inhibited. On the other hand, administration of moderate
concentration of T4 to TU-treated larvae completed eye migration (Miwa
and Inui, 1987b). In addition, eye migration can be initiated by exogenous
T4 in premetamorphic larvae. TU treatment did not completely deplete
tissue T4 of the whole body (unpublished data). These results indicate
that eye migration starts with a low level of T4, but a higher level of T4 is
required for the completion of the migration. Thus, it seems that, also in
the fl ounder, different tissues need different levels of T4 for the initiation
of metamorphic process and that different levels of thyroid hormone are
needed for the sequence of metamorphic change in each organ.
4.2.4 Pituitary-thyroid axis and its negative feedback regulation:
effects of exogenous TSH
The activation of pituitary TSH cells in metamorphosis strongly suggests
that TSH induces the surge of thyroid hormone in metamorphic climax
in the Japanese fl ounder. To confi rm this, Inui et al. (1989) injected bovine
TSH to prometamorphic fl ounder larvae. TSH injection increased tissue
T4 concentration in a dose-dependent manner, though the injection
did not affect tissue T3 concentration. A single injection of TSH of a
supposedly physiological dose increased tissue T4 level to the similar
level of metamorphic climax (Fig. 6), and duplicate injections of TSH with
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