Does raising the level of thyroid hormone in the fetus by itself accelerate gene expression?
	We first considered the possibility that the response to T3 is conditioned by the surge in T3 itself. We have addressed this question by injection of 2.5 mg of T4/100 gbw on gestational day 14 in a hypothyroid rat. This resulted in sufficient transplacental transport of hormone to raise the concentration of T3 in the fetal brain on the day of birth to a level comparable to that in a normal adult. However, there was no premature expression of Pcp-2, myelin basic protein, or CamKIV, a brain gene which has recently been reported to be a T3 target. Neither did we advance the developmental schedule of the cerebellum. These findings argue against the possibility that a rise in T3 triggers the initiating process.