THYROID-HORMONE RECEPTORS AND LODOTHYRONINE DEIODINASES IN THE DEVELOPING MEXICAN AXOLOTL, AMBYSTOMA-MEXICANUM

The Mexican axolotl, Ambystoma mexicanum, is a neotenous salamander that rarely undergoes anatomical metamorphosis, but can be induced to do so by administration of thyroxine (T4). The neoteny appears to be due primarily to low levels of plasma T4 secondary to a low rate of secretion of thyroid-stimulating hormone. However, other factors may also be involved. In anuran amphibia, metamorphosis is accompanied by alterations in thyroid hormone receptor concentration and marked changes in the activities of the iodothyronine deiodinase systems, all of which contribute to enhancing peripheral sensitivity to circulating T4. The present study was designed to assess these functions in the tissues of the axolotl. Putative 3,5,3′-triiodothyronine (T3) receptors were readily detected in axolotl red blood cells, and the receptor number (sites/nucleus) showed a developmental decline, comparable to that seen in anuran amphibia, as the larval cells with a high receptor number were replaced with adult cells with a low receptor number. Saturable T3 nuclear binding sites were also detected in liver, but the receptor number was too low to quantitate. Using a sensitive RIA, T4 and T3 were below detectable levels in juvenile axolotls and T4 was just detectable in some of the adults. Following injection of [125I]T4, [125I]T3 was detected in plasma and liver of adult, but not of juvenile, axolotls. Some 5′-deiodinase activity was consistently detected in preparations of larval skin, and in adult skin and gut, but it was too low to permit kinetic analyses. Activity was not increased following treatment with sufficient T4 to induce anatomical metamorphosis. 5-Deiodinase activity was not detected in any tissue. The studies support the concept that the major cause of anatomical neoteny in the axolotl is an inadequate plasma T4 concentration. They also suggest that axolotl tissues, unlike those of anuran amphibia, do not undergo some of the specific changes which would be expected to enhance the physiological response to the available T4. © 1992.