218
J. N. BALL
by prolactin, but not by MSH or by ACTH (which appears to promote
melanogenesis in the goldfish; Chavin, 1956, 1959). Prolactin did not
cause proliferation of new melanophores, but intermedin (MSH) did
cause melanophore proliferation, and its action was potentiated by prolactin. Thus melanogenesis and melanophore proliferation are separable
in F . heteroclitus on the basis of their responses to prolactin and MSH
(Pickford and Kosto, 1957). In extending this work, it was found that
dopa tyrosinase activity in fin tissue in vitro decreased after hypophysectomy (this being an essential enzyme in the pathway of melanin synthesis) and that enzymic activity was restored by prolactin, which also
restored melanin pigmentation in viuo; however, in vitro restoration of
dopa tyrosinase activity is not necessarily correlated with restoration of
in vivo pigmentation, since ACTH and MSH also restored the in oitro
activity without affecting in vivo melanogenesis. In interpreting their
finding, Kosto et aZ. (1959) suggested that the unique ability of prolactin
to restore the melanin content of faded melanophores may lie in an action
that makes available some melanin precursor, the supply of which is deficient after hypophysectomy. They also emphasized that prolactin appeared to increase the dopa tyrosinase activity of preexisting melanophores, whereas ACTH and MSH primarily increased the number of
melanophores, each probably with only a low level of enzymic activity.
These results demonstrate definitely an effect of ovine prolactin in
promoting melanogenesis in Fundulus and differentiate this action from
the proliferative effects of MSH (and, to a minor extent, ACTH). The
distribution of this prolactin effect in teleosts is not known. Work on the
goldfish (Chavin, 1956, 1959) indicates that in this species it is ACTH,
not prolactin, that stimulates melanin synthesis. It seems likely that impairment of melanin formation after hypophysectomy is general in teleosts, although sometimes obscured by the persistence of neural mechanisms for background adaptation, and sometimes not apparent because
of too short a period of observation after the operation (see Pickford and
Atz, 1957). In the author’s laboratory P. latipinna has repeatedly been
observed to develop pallor after hypophysectomy, associated with depletion of measurable melanin in the dorsal skin; the pituitary factors involved are still under investigation, but it can be said that ovine prolactin
restores melanin after hypophysectomy in this species as in F. heteroclitus. Curiously, beef prolactin did not induce melanogenesis in hypophysectomized F . heteroclitus, although primate growth hormone, with intrinsic prolactin activity, did exhibit melanogenic potency ( Pickford et
al., 1965). Ovine prolactin caused melanodispersion in the eel, even after
hypophysectomy, and may also stimulate melanogenesis ( Olivereau,
1!366) I
J. N. BALL
by prolactin, but not by MSH or by ACTH (which appears to promote
melanogenesis in the goldfish; Chavin, 1956, 1959). Prolactin did not
cause proliferation of new melanophores, but intermedin (MSH) did
cause melanophore proliferation, and its action was potentiated by prolactin. Thus melanogenesis and melanophore proliferation are separable
in F . heteroclitus on the basis of their responses to prolactin and MSH
(Pickford and Kosto, 1957). In extending this work, it was found that
dopa tyrosinase activity in fin tissue in vitro decreased after hypophysectomy (this being an essential enzyme in the pathway of melanin synthesis) and that enzymic activity was restored by prolactin, which also
restored melanin pigmentation in viuo; however, in vitro restoration of
dopa tyrosinase activity is not necessarily correlated with restoration of
in vivo pigmentation, since ACTH and MSH also restored the in oitro
activity without affecting in vivo melanogenesis. In interpreting their
finding, Kosto et aZ. (1959) suggested that the unique ability of prolactin
to restore the melanin content of faded melanophores may lie in an action
that makes available some melanin precursor, the supply of which is deficient after hypophysectomy. They also emphasized that prolactin appeared to increase the dopa tyrosinase activity of preexisting melanophores, whereas ACTH and MSH primarily increased the number of
melanophores, each probably with only a low level of enzymic activity.
These results demonstrate definitely an effect of ovine prolactin in
promoting melanogenesis in Fundulus and differentiate this action from
the proliferative effects of MSH (and, to a minor extent, ACTH). The
distribution of this prolactin effect in teleosts is not known. Work on the
goldfish (Chavin, 1956, 1959) indicates that in this species it is ACTH,
not prolactin, that stimulates melanin synthesis. It seems likely that impairment of melanin formation after hypophysectomy is general in teleosts, although sometimes obscured by the persistence of neural mechanisms for background adaptation, and sometimes not apparent because
of too short a period of observation after the operation (see Pickford and
Atz, 1957). In the author’s laboratory P. latipinna has repeatedly been
observed to develop pallor after hypophysectomy, associated with depletion of measurable melanin in the dorsal skin; the pituitary factors involved are still under investigation, but it can be said that ovine prolactin
restores melanin after hypophysectomy in this species as in F. heteroclitus. Curiously, beef prolactin did not induce melanogenesis in hypophysectomized F . heteroclitus, although primate growth hormone, with intrinsic prolactin activity, did exhibit melanogenic potency ( Pickford et
al., 1965). Ovine prolactin caused melanodispersion in the eel, even after
hypophysectomy, and may also stimulate melanogenesis ( Olivereau,
1!366) I