1. THE PITUITARY GLAND
49
in part at least attributable to carp TSH in the extracts (Olivereau,
1967a). It is perhaps worth recalling that the question of whether or not
sexual maturation in teleosts is necessarily accompanied by thyroidal
hyperactivity is still open, with conflicting reports in the literature (see
Pickford and Atz, 1957; Ball, 1960).
Eel TSH cells were not modified 8 or 9 days after surgical interrenalectomy (Olivereau and Olivereau, 1968) but were quite strongly activated after 2-5 days treatment with the adrenocortical inhibitor SU 4885
(cf. Section 11, B, 2 ) , and SU 4885 also activates the TSH cells after 5
days’ treatment in Poecilia, although not at 2 days (Ball and Olivereau,
1966).
An unexpected reaction of the TSH cells of the eel occurs in response
to injections of ovine prolactin. Olivereau (1966b) found that chronic
injections of prolactin resulted in marked histological activation of the
thyroid in intact eels but not of hypophysectomized animals. After only
2 or 3 daily injections, the TSH cells in the intact animals were slightly
hypertrophied, with occasional mitoses, and with further injections the
TSH cells in the intact animals became extremely activated and displayed
many mitoses. As Olivereau pointed out, the effects of the exogenous
prolactin could result from its acting as a goitrogen, preventing the formation of thyroid hormone and, hence, by removing feedback inhibition,
resulting in elevated TSH output; or, the ovine prolactin could somehow
be causing eIevated TSH output even in the presence of a normally functional thyroid, as if it were acting like a TSH-releasing factor. A similar
action of ovine prolactin on the TSH-thyroid axis in the amphibian Rana
catesbiana appears to represent a goitrogenic effect (Gona, 1967), although this is not apparently true for thyroidal stimulation by prolactin
in a urodele (Vellano et al., 1967). Subsequent work on the eel
(Olivereau, 1969c) showed that prolactin does not act like a goitrogen in
this case, since in addition to the histological signs of thyroidal activation,
prolactin also increased l3II uptake by the gland; thus, the activation of
the eel TSH cells by ovine prolactin presumably depends on some hypothalamic or intrapituitary mechanism not yet understood.
Atz (1953) observed striking changes in the thyrotrops of Astyanax
following injections of cortisone or ACTH daily for 10 days. The TSH
cells underwent a cycle of degranulation and vacuolation followed by
regranulation, both at the beginning and the end of the injection period,
and also displayed mitotic activity. The fact that similar effects were produced by daily saline injections suggests that Atz was observing a response to stress normally mediated by the ACTH-adrenal axis.
The TSH cells are better granulated in eels in seawater than in freshwater animals ( Olivereau and Olivereau, 1968), probably indicating a
49
in part at least attributable to carp TSH in the extracts (Olivereau,
1967a). It is perhaps worth recalling that the question of whether or not
sexual maturation in teleosts is necessarily accompanied by thyroidal
hyperactivity is still open, with conflicting reports in the literature (see
Pickford and Atz, 1957; Ball, 1960).
Eel TSH cells were not modified 8 or 9 days after surgical interrenalectomy (Olivereau and Olivereau, 1968) but were quite strongly activated after 2-5 days treatment with the adrenocortical inhibitor SU 4885
(cf. Section 11, B, 2 ) , and SU 4885 also activates the TSH cells after 5
days’ treatment in Poecilia, although not at 2 days (Ball and Olivereau,
1966).
An unexpected reaction of the TSH cells of the eel occurs in response
to injections of ovine prolactin. Olivereau (1966b) found that chronic
injections of prolactin resulted in marked histological activation of the
thyroid in intact eels but not of hypophysectomized animals. After only
2 or 3 daily injections, the TSH cells in the intact animals were slightly
hypertrophied, with occasional mitoses, and with further injections the
TSH cells in the intact animals became extremely activated and displayed
many mitoses. As Olivereau pointed out, the effects of the exogenous
prolactin could result from its acting as a goitrogen, preventing the formation of thyroid hormone and, hence, by removing feedback inhibition,
resulting in elevated TSH output; or, the ovine prolactin could somehow
be causing eIevated TSH output even in the presence of a normally functional thyroid, as if it were acting like a TSH-releasing factor. A similar
action of ovine prolactin on the TSH-thyroid axis in the amphibian Rana
catesbiana appears to represent a goitrogenic effect (Gona, 1967), although this is not apparently true for thyroidal stimulation by prolactin
in a urodele (Vellano et al., 1967). Subsequent work on the eel
(Olivereau, 1969c) showed that prolactin does not act like a goitrogen in
this case, since in addition to the histological signs of thyroidal activation,
prolactin also increased l3II uptake by the gland; thus, the activation of
the eel TSH cells by ovine prolactin presumably depends on some hypothalamic or intrapituitary mechanism not yet understood.
Atz (1953) observed striking changes in the thyrotrops of Astyanax
following injections of cortisone or ACTH daily for 10 days. The TSH
cells underwent a cycle of degranulation and vacuolation followed by
regranulation, both at the beginning and the end of the injection period,
and also displayed mitotic activity. The fact that similar effects were produced by daily saline injections suggests that Atz was observing a response to stress normally mediated by the ACTH-adrenal axis.
The TSH cells are better granulated in eels in seawater than in freshwater animals ( Olivereau and Olivereau, 1968), probably indicating a