The role of the lizard thyroid gland in tail regeneration.

Abstract

AbstractHypothyroidism in Anolis carolinensis caused almost a two week delay in blastema formation and tail elongation was completely inhibited. Hormonal replacement therapy (L‐thyroxine) in hypothyroid lizards allowed for normal blastema formation as well as subsequent tail elongation.Hyperthyroidism in Anolis initiated the early development and subsequently the early completion of blastema formation but had no significant effect on tail elongation.Histological observations in the hypothyroid regenerates when compared with those receiving thyroxine replacement revealed that: (a) the inhibition of tail elongation was due to an inhibition of the outgrowth of the ependyma into the developing blastema; (b) although tail elongation was inhibited in hypothyroid lizards, many tissues within the blastema did differentiate along the same time course as those found in hormonal replacement regenerates and controls; thus, thyroxine apparently had little to do with tissue differentiation in these animals.Hypophysectomy was found to delay blastema formation by one and one‐half weeks and to inhibit tail elongation in the same manner as was found in hypothyroid lizards. A dose response relationship was found to exist between certain levels of thyroxine (0.04 to 0.2 μg) and tail regeneration in hypophysectomized lizards. The intermediate dose of thyroxine (0.2 μg) produced a maximum response with respect to lizard tail elongation. A greater dose of thyroxine (1.0 μg) did not further augment the regeneration process and any greater dose would likely produce an inhibitory effect.