Developmental and ploidy characteristics of "senescent" unfertilized eggs of Xenopus laevis.

Unfertilized eggs of Xenopus laevis have been stored in a high salt physiological saline (De Boer's solution) over a period of about 24 hours. During this time, aliquots have been subjected to lowered salinity and fertilized. The stored eggs undergo a defined series of morphological changes, which are initially reversible upon fertilization. Length of storage may have little or no effect on the capacity of the eggs to undergo cleavage, but the normal developmental capacity declines with increasing storage time. Among the characteristics of this decline is a regressive cytokinesis, early arrest, and the appearance in surviving larvae of a definable syndrome of morphological type. Increasing storage times predispose the eggs to subsequent triploid development, the triploidy arising as a consequence of failure of second polar body emission. The possible interest of these findings for a model system of mammalian gamete aging is discussed.

The response of the brachial ventral horn or Xenopus laevis to forelimb amputation during development.

The normal development of the brachial ventral horn of the frog Xenopus laevis and the response of the brachial ventral horn to complete forelimb extirpation at five developmental stages were assessed histologically. Differentiation of brachial ventral horn neurons occurred in pre-metamorphic tadpoles between stages 52/53 and 57. Mean cell number in the brachial ventral horn reached a peak of 2576 (S.E.M. equals +/- 269, N equals 2) per side of the spinal cord at stage 55 and decreased to 1070 (S.E.M. equals +/- 35, n equals 7) by the end of metamorphosis. Cell degeneration was presumed to be the mode of cell loss since it was most prevalent during the period of rapid decrease in cell numbers. The response of the ventral horn to forelimb removal varied with the stage of the animal at amputation. Following amputation at stage 52/53 or 54 the ipsilateral ventral horn neurons appeared less differentiated than those on the control side and a rapid cell loss of about 80% occurred on the operated side. These effects occurred more rapidly after ablation at stage 54 than at stage 52/53. Amputation at stage 58, 61, or 66 caused chromatolysis in the ventral horn, a period of relative cell excess on the operated side, and a delayed neuronal loss of 32-66%. It was concluded that excess cell degeneration accounted for cell loss and that suppression of normal neuronal degeneration caused the relative cell excess on the operated side. The data indicate that the brachial ventral horn was indifferent to the periphery before stage 54, was quickly affected by limb removal between stages 54 and 58, and by stage 58 had entered a phase in which a delay preceded cell death. No forelimb regeneration occurred.