4. THYROID FUNCTION AND ITS CONTROL IN FISHES
243
(Gorbman et al., 1963; Gorbman, 1965). In elasmobranchs, a large part
of the TSH is said to be formed in the ventral lobe, an extension of the
pars distalis that appears to have no anatomical connection with the brain
(Dodd et al., 1963). In teleosts, on the other hand, there is an interdigitation of the neurohypophysis and adenohypophysis. Accordingly, in teleosts there seems to exist the possibility for the brain to influence the
adenohypophysis either through a vascular route or by direct innervation
(M. Fontaine and Leloup, 1964; Stahl and Leray, 1961). Which of these
is utilized is not known.
Although an anatomical means for hypothalamic control over TSH (or
other tropic hormones) appears to be absent in cyclostomes, there is some
evidence that it may still occur, possibly through the secretion of hypothalamic releasing factors into the systemic circulation. For example,
continuous illumination of ammocoetes larvae of lampreys affects stainable hypothalamic neurosecretion ( Oztan and Gorbman, 1960a,b ). Purely
circumstantial evidence resides in the fact that thyroid gland metamorphosis and sexual maturation of larval lampreys are closely linked to
season. Finally, there is dubious evidence based on the hyperplasia of
ammocoetes endostyle ( larval thyroid) epithelium following treatment
with goitrogenic drugs (Klenner, 1952; Olivereau, 1956; Barrington and
Sage, 1963,1966)- In higher vertebrates, at least, goitrogens act by blocking thyroid hormone synthesis, and the resulting lowered level of thyroid
hormone in blood evokes TSH secretion. Unfortunately, the possibility
that ammocoete endostylar hypertrophy is evoked in this way seems
denied by recent experiments of Barrington and Sage ( 1966). They found
that hypophysectomy will not prevent the “goitrogenic” effect of thiourea,
thus this hyperplasia in lampreys cannot result from evoked TSH
secretion.
For elasmobranchs, also, information concerning control of TSH secretion is almost completely absent. In these forms there is a well-developed,
frequently double median eminence and a portal system of vessels connecting this part of the hypothalamus with the pars distalis (Follenius,
1965; Mellinger, 1963; Meurling, 1960). Yet, as has been mentioned, Dodd
et al. (1963) have reported that a special adenohypophysial structure of
elasmobranchs that produces TSH (the ventral lobe of the pars distalis)
is not related to this portal system. Olivereau (1951) has reported that
goitrogens do not alter thyroidal histology in sharks, so that feedback
control through the hypothalamus or direct pituitary sensitivity to blood
thyroxine may also be lacking in these forms. The TSH secretory mechanism remains unstimulated in goitrogenized Scyliorhinzrs despite the fact
that it can be shown that the goitrogen is in fact blocking iodine metabolism in the thyroid (Leloup, 1952). In contrast to these results, Pritchard
243
(Gorbman et al., 1963; Gorbman, 1965). In elasmobranchs, a large part
of the TSH is said to be formed in the ventral lobe, an extension of the
pars distalis that appears to have no anatomical connection with the brain
(Dodd et al., 1963). In teleosts, on the other hand, there is an interdigitation of the neurohypophysis and adenohypophysis. Accordingly, in teleosts there seems to exist the possibility for the brain to influence the
adenohypophysis either through a vascular route or by direct innervation
(M. Fontaine and Leloup, 1964; Stahl and Leray, 1961). Which of these
is utilized is not known.
Although an anatomical means for hypothalamic control over TSH (or
other tropic hormones) appears to be absent in cyclostomes, there is some
evidence that it may still occur, possibly through the secretion of hypothalamic releasing factors into the systemic circulation. For example,
continuous illumination of ammocoetes larvae of lampreys affects stainable hypothalamic neurosecretion ( Oztan and Gorbman, 1960a,b ). Purely
circumstantial evidence resides in the fact that thyroid gland metamorphosis and sexual maturation of larval lampreys are closely linked to
season. Finally, there is dubious evidence based on the hyperplasia of
ammocoetes endostyle ( larval thyroid) epithelium following treatment
with goitrogenic drugs (Klenner, 1952; Olivereau, 1956; Barrington and
Sage, 1963,1966)- In higher vertebrates, at least, goitrogens act by blocking thyroid hormone synthesis, and the resulting lowered level of thyroid
hormone in blood evokes TSH secretion. Unfortunately, the possibility
that ammocoete endostylar hypertrophy is evoked in this way seems
denied by recent experiments of Barrington and Sage ( 1966). They found
that hypophysectomy will not prevent the “goitrogenic” effect of thiourea,
thus this hyperplasia in lampreys cannot result from evoked TSH
secretion.
For elasmobranchs, also, information concerning control of TSH secretion is almost completely absent. In these forms there is a well-developed,
frequently double median eminence and a portal system of vessels connecting this part of the hypothalamus with the pars distalis (Follenius,
1965; Mellinger, 1963; Meurling, 1960). Yet, as has been mentioned, Dodd
et al. (1963) have reported that a special adenohypophysial structure of
elasmobranchs that produces TSH (the ventral lobe of the pars distalis)
is not related to this portal system. Olivereau (1951) has reported that
goitrogens do not alter thyroidal histology in sharks, so that feedback
control through the hypothalamus or direct pituitary sensitivity to blood
thyroxine may also be lacking in these forms. The TSH secretory mechanism remains unstimulated in goitrogenized Scyliorhinzrs despite the fact
that it can be shown that the goitrogen is in fact blocking iodine metabolism in the thyroid (Leloup, 1952). In contrast to these results, Pritchard