Biology Reference
In-Depth Information
2.1. Thyroid-stimulating hormone
Hypophysectomy of tadpoles arrests the development of the thyroid gland
and leads to metamorphic stasis that is reversed by injecting TSH (
Dodd &
Dodd, 1976; Regard & Mauchamp, 1971, 1973
). The rate of thyroid gland
growth and TH production in the tadpole is coordinate with the develop-
ment of the pituitary and the production of TSH (
Buckbinder & Brown,
1993; Denver, 1996; Dodd & Dodd, 1976; Kaye, 1961; Korte et al.,
2011; Manzon & Denver, 2004; Okada et al., 2009, 2004
). The amphibian
thyroid gland develops sensitivity to TSH just before hatching (
Kaye, 1961
).
Pituitary expression of
tsh
b
mRNA and plasma TSH concentration in-
creases throughout metamorphosis (
Buckbinder & Brown, 1993; Manzon
& Denver, 2004; Okada et al., 2000
). Pituitary
tsh
b
mRNA levels rise from
premetamorphosis to peak values during late prometamorphosis/metamor-
phic climax (
Buckbinder & Brown, 1993; Manzon & Denver, 2004;
Okada et al., 2000
).
Korte et al. (2011)
used a homologous radioimmunoassay
to show that changes in plasma and pituitary TSH in
Xenopus
species through-
out metamorphosis paralleled changes in pituitary
tsh
b
mRNA. Thus, TSH
biosynthesis is coordinate with thyroid gland development and hormone se-
cretion, and the stimulatory action of pituitary TSH is necessary for thyroid
gland growth and hormone biosynthesis.
The tripeptide amide thyrotropin-releasing hormone (TRH), which is
the primary regulator of TSH release in adult mammals, is inactive on tad-
pole TSH secretion, although the
trh
gene is expressed in the brain and pi-
tuitary of amphibians (
Denver, 1996; Denver & Licht, 1989; Kikuyama
et al., 1993; Manzon & Denver, 2004; Norris & Dent, 1989; Okada
et al., 2004
), and TRH can stimulate TSH release in adult frogs (
Denver,
2009a; Galas et al., 2009
). Many studies now support that the secretion of
TSH by the tadpole pituitary gland is under stimulatory control by
corticotropin-releasing factor (CRF) and related peptides (e.g., sauvagine,
urocortins;
Denver, 2009b, 2009c
). CRF-like peptides regulate neuroendo-
crine, autonomic, and behavioral responses to physical and emotional stress
(
Aguilera, 1998; Yao & Denver, 2007
).
CRF was named for its role in inducing release of pituitary ACTH in
mammals, a role that is shared in amphibia (
Vale, Vaughan, & Perrin,
1997
). Shortly after its discovery in 1981, CRF was discovered to be a potent
stimulator of the thyroid axis in larval amphibians and other nonmammalian
vertebrates (
De Groef, Van der Geyten, Darras, & Kuhn, 2006; Denver,
1999, 2009b, 2009c
). Treatment of amphibian pituitary explants or primary
pituitary cells with CRF-like peptides stimulated TSH release (
De Groef
