Biology Reference
In-Depth Information
tissues and has been applied to mature tissues such as the brain (
Greenberg
et al., 2006
), but not to the authors' knowledge to the developing embryo.
Human thyroid gland development starts to develop at the day 24 of ges-
tation. At that time, the embryonic thyroid is visible as a bulge in the pha-
ryngeal floor. Then, the thyroid gland tissues merge and migrate to their final
location. By gestational day 74, the thyroid gland starts to concentrate iodide
and produce MIT, DIT, T
4
, and T
3
(
Shepard, 1967
).
In the free-living
X. laevis
embryo, the thyroid gland forms between
stages NF40 and NF45 (
Jayatilaka, 1978
) with visible follicles at NF46
(about 1 week of age in standard rearing conditions). In zebrafish, the thy-
roid gland forms at 40 hpf (
Rohr & Concha, 2000
), but the use of radioac-
tive iodine uptake shows that endogenous production of THs starts at 3 dpf
in zebrafish (
Brown, 1997
). The origin of TH present in embryo has there-
fore to be investigated, as thyroid gland only become active in late
development.
3.1. T
3
and T
4
are maternally provided in mammals
THs, T
4
and T
3
, are essential for normal physiology and development in all
vertebrates, with particularly marked effects on metamorphosis and brain
development in mammals (
Bernal, 2007; Hamburgh, 1969; Lezoualc'h
et al., 1995
). Traditionally, research in human and rodents has focused on
what appears to the most sensitive period, usually the period of most rapid
brain growth, which in humans is that early postnatal period.
However, during pregnancy many changes occur in maternal TH me-
tabolism. Peripheral metabolism of TH and serum TH distributor protein
production increase during this time. Notably, there is a huge increase in
free thyroxin during the first trimester followed a decrease to reach levels
of a nonpregnant woman (
Burrow, Fisher, & Larsen, 1994
). In parallel, total
T
4
and protein distributors (thyroid binding globulin TBG and transthyretin
TTR) also increase significantly during the first trimester and remain high
until delivery (
Burrow et al., 1994; Glinoer, 2000
). Interestingly, in hypo-
thyroid mothers treated before becoming pregnant, the dose of T
4
given to
fit the demand has to be increased by 25-50% to maintain normal serum
thyrotropin concentrations during pregnancy (
Kaplan, 1992b; Mandel,
Hanna, & LaFranchi, 1990
). Thus, the total (free and bound-to-serum
protein) levels of maternal T
4
and T
3
increase during pregnancy, whereas
the maternal level of free T
4
remains constant (
Contempre et al., 1993;
Kaplan, 1992a
) due to the increase in distributor proteins.
