Neuronal overload in the developing anuran lateral motor column in response to limb removal and thyroid hormone.

The lateral motor column (LMC) in the anuran spinal cord normally undergoes a dramatic reduction in motor neuron number during development. At least two factors influence this process: the limb target which is required for the progression of cell loss, and thyroid hormone, a requisite for metamorphosis. This study has examined the relative and combined effects of limb amputation and exogenous thyroxine, initiated at the onset of normal rapid cell loss in Rana pipiens tadpoles, in regulating neuron number in the lumbosacral LMC. Thyroxine treatment or unilateral limb amputation temporarily resulted in significantly more LMC neurons than in untreated controls. Extraordinary numbers of motor neurons persisted through metamorphic climax when both treatments were combined. Population sizes frequently exceeded the maximum number of neurons observed prior to the onset of natural cell loss. Moreover, thyroxine-treated tadpoles contained increased numbers of mitotic figures in the ventricular zone of the spinal cord and significantly more newly generated cells in the LMC, as revealed by 3H-thymidine autoradiography. These findings suggest that thyroxine-potentiated mitogenesis promotes greater numbers of new motor neurons to the LMC while, simultaneously, target removal delays the loss of extant cells. It is proposed that this interaction effectively maintains an immature state in the LMC so that neuronal "decisions" for survival and the consequent loss of target-deprived neurons are postponed far longer than previously reported.