Abstract
The lid-closure (wink) reflex of amphibians—retraction of the eye bulb upon tactile stimulation of the cornea or surrounding skin—appears comparatively late in development. Urodeles display it first in advanced larval stages, anurans at or about the time of metamorphic climax. In the latter group its dependence upon the metamorphosing agents was demonstrated by experiments in which metamorphosis was either suppressed (hypophysectomy) or advanced (hyperthyroidism); 1 in the former case, the reflex failed to appear unless thyroid was administered, while in the latter case its onset was advanced almost, though not fully, as much as was the transformation of the body. Both the sensory (trigeminal) and motor (abducens) components of the reflex develop full functional capacity in very early larval stages, but their central linkage into a workable reflex mechanism is not effected until at the time of metamorphosis.
The close association with metamorphosis suggested that maturation of the central mechanism of the reflex might be under direct control of the thyroid hormone. In order to test this possibility, an attempt was made to precipitate the development of the reflex relative to the metamorphic changes in the rest of the body by exposing the hind brain locally to supernormal concentrations of the hormone. As Hartwig 2 has shown, implantation of thyroxin-soaked agar under the fin skin of salamander larvae causes local metamorphosis of the surrounding tissues. A similar procedure was, therefore, adopted for the present experiments.
Agar pellets were soaked in thyroxin (1:1000) and then implanted into the fourth ventricle of tadpoles of Rana pipiens.
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