Biology Reference
In-Depth Information
Kasai, 2003
). A role for GH in regulating body growth in amphibia as in
other vertebrates (
Harvey et al., 1995
) has been demonstrated by many
studies in which GH was injected into tadpoles or frogs (
Denver, 1996;
Kikuyama et al., 1993; White & Nicoll, 1981
) and more recently through
transgenic overexpression of GH in
X. laevis
(
Huang & Brown, 2000a
).
In contrast to GH, a role for PRL in regulating tadpole growth and meta-
morphosis continues to be controversial (
Huang & Brown, 2000b
). Early
work supporting that PRL inhibited metamorphosis and stimulated larval
growth was conducted with mammalian PRL (and GH) preparations. These
studies clearly showed that functional receptors for PRL/GH are expressed in
amphibian tissues and their activation can both promote tadpole growth and
block T
3
-induced metamorphosis; the latter action likely through the preven-
tion of
TR
b
autoinduction (
Tata, Baker, Machuca, Rabelo, & Yamauchi,
1993
). Further, injection of purified frog PRL had similar effects on tadpole
growth and development as mammalian PRL (
Kikuyama et al., 1993
).
One can argue that the effects of exogenous hormones may represent
pharmacological rather than physiological actions. However, it is notewor-
thy that blockade of endogenous PRL by passive immunization accelerated
metamorphic changes, which supports a physiological role for the endoge-
nous hormone (
Denver, 1996; Kikuyama et al., 1993
).
Etkin (1968)
pro-
posed that larval growth and metamorphosis is controlled by a balance
between TH and PRL, and that the two should show an inverse relationship
in their blood concentrations at metamorphic climax. The rise in circulating
concentrations of TH during prometamorphosis and climax have been con-
firmed (see above). However, circulating concentrations of PRL and levels
of pituitary
prl
mRNA are low during premetamorphosis and also rise, more
or less in parallel with TH, during late prometamorphosis and climax
(
Buckbinder & Brown, 1993; Clemons & Nicoll, 1977; Niinuma,
Yamamoto, & Kikuyama, 1991; Takahashi et al., 1990; Yamamoto &
Kikuyama, 1982
), thus contradicting the earlier hypothesis of an inverse re-
lationship of the two hormones (
Etkin, 1968
). The rise in PRL production
tends to occur slightly later than the rise in TSH expression and circulating
TH (
Buckbinder & Brown, 1993
). Similarly, [
125
I]-PRL binding to kidney
membrane fractions was low in premetamorphic bullfrog tadpoles and in-
creased during metamorphic climax (
White & Nicoll, 1979
).
Huang and
Brown (2000b)
measured PRL receptor mRNA in whole
X. laevis
tadpole
and tail tissue and found increased expression at metamorphic climax.
Hasunuma, Yamamoto, and Kikuyama (2004)
found that PRL receptor
mRNA increased in the tail fin and kidney of bullfrog tadpoles during
