Biology Reference
In-Depth Information
by tadpole interrenal glands prior to the onset of metamorphosis
(
Glennemeier & Denver, 2002a
). Premetamorphic tadpoles are capable of
mounting a CORT response following exposure to a physical stressor (shak-
ing/confinement stressor;
Glennemeier & Denver, 2002a
), which suggests
that functional maturation of the hypothalamo-hypophyseal-interrenal axis
occurs prior to metamorphosis (by contrast to the tadpole hypothalamo-
hypophyseal-thyroid axis, which matures during prometamorphosis). The
early functional maturation of the hypothalamo-hypophyseal-interrenal
axis is reflected in the earlier expression of the CRF
1
receptor (expressed
on corticotropes; expression at NF stage 52) compared with the CRF
2
receptor (expressed on thyrotropes; expression at NF stage 57) (
Manzon
& Denver, 2004; Okada et al., 2009
;
Fig. 7.2
). The early maturation of
the hypothalamo-hypophyseal-interrenal axis provides for environmental
stressors to elevate endogenous CS production in premetamorphic tadpoles,
which can have consequences for tadpole growth and development.
Compared with TSH, much less is known about how the hypothalamus
controls ACTH secretion in amphibia. CRF and arginine vasopressin (AVT
is the amphibian hormone) have been shown to stimulate ACTH secretion
by cultured adult frog pituitaries (
Tonon et al., 1986
).
2.3. Growth hormone and prolactin
A central prediction of Etkin's model for the endocrine control of tadpole
metamorphosis (
Etkin, 1968
) was that the metamorphic actions of TH were
balanced by the inhibitory actions of the pituitary hormone prolactin (PRL).
Etkin proposed that in the premetamorphic tadpole, PRL secretion was
high, but declined at metamorphic climax. This prediction was based in large
part on the inhibitory effects of injecting mammalian PRLs on metamorphosis
(
White & Nicoll, 1981
), which led some investigators to suggest that PRL
exerted a juvenilizing action in amphibian larvae similar to juvenile hormone
in insects (
Bern, Nicoll, & Strohman, 1967; Etkin & Gona, 1967
).
The early studies that led to the development of the Etkin model have
been extensively reviewed (
Denver, 1996; Dodd & Dodd, 1976;
Kaltenbach, 1996; Kikuyama et al., 1993; White & Nicoll, 1981
). Work
using mostly mammalian PRL or GH preparations suggested different roles
for these hormones, with PRL enhancing larval growth and blocking the
actions of TH on metamorphosis, and GH stimulating postmetamorphic
growth as the hormone does in most vertebrates (
Denver, 1996; Takada &
