Reduction in cell size during development of the spinal cord

Abstract

During development, spinal cord cells of the frog Xenopus laevis undergo a reduction in size. This phenomenon occurs during neural tube formation and continues at least until the start of metamorphosis. The number and shape of spinal cord cells also changes, but not always in synchrony with the reduction in cell size. The concomitant change in size and number of spinal cord cells during embryogenesis suggests that a cleavage type of reductive division contributes to the decrease in cell size. Blocking cell division with a combination of hydroxyurea and aphidicolin (HUA) stops the decrease in cell size during embryonic development without affecting the differentiation of a specific class of catecholaminergic neurons. HUA treatment during larval stages does not block the decrease in catecholaminergic neuron size. Thus, both mitotic and postmitotic cells decrease in size during spinal cord development. The two mechanisms are prevalent at different developmental stages with reductive division and cellular atrophy common during embryonic and larval phases, respectively. Like other regressive changes such as cell death and synapse elimination, decreases in cell size affect spinal cord morphogenesis and presumably the function of developing spinal cord cells. J. Comp. Neurol. 409:592–602, 1999. © 1999 Wiley‐Liss, Inc.

Thyroid hormone promotes neurogenesis in the Xenopus spinal cord

“…Our results taken together with previous studies (Lamborghini, 1980;Thors et al, 1982a,b;van Mier, 1986;Hartenstein, 1989Hartenstein, , 1993Chen et al, 1999) allow us to define three phases of Xenopus spinal cord development (Fig. 1).…”

“…The two layers of the neuroectoderm have interdigitated and now form an unilayered and pseudostratified epithelium (Schroeder, 1970;Davidson and Keller, 1999), in which the mitotic nuclei are confined to the ventricular surface (Hartenstein, 1989). There is no increase in the diameter of the spinal cord throughout this period (Thors et al, 1982a;Chen et al, 1999), because increase in cell number due to low-level proliferation (Hartenstein, 1989;Chen et al, 1999) is largely compensated for by decrease in cell size (Chen et al, 1999). From stage 35/36 onward, rates of cell proliferation further decline (Chen et al, 1999) reflected in reduced levels of XNeuroD and XMyT1 expression from stage 37/38 onward.…”

“…1). Neurogenesis continues at later embryonic stages, when mainly interneurons are born (Hartenstein, 1989;Chen et al, 1999;Binor and Heathcote, 2001). After a quiescent period, the majority of secondary neurons, such as the motor neurons of the lateral motor columns, the sensory dorsal root ganglion cells, as well as many spinal interneurons, are then born during a larval period of neurogenesis (Fig.…”

“…The hatched black line provides a rough sketch of interneuron generation. The time course of interneuron generation rates before stage 48 is unknown (question marks), but average rates between stage 22 and stage 37/38 can be estimated from interneuron counts provided by Roberts (1989), rates between stage 37/38 and 46 must be lower (Chen et al, 1999), whereas at later stages, rates and numbers relative to motor neurons can be estimated from Thors et al (1982b). No reliable information is available on neuron generation rates at stages later than stage 53 (LMC, DRG) or 56 (interneurons).…”

Establishment of a ventral cell fate in the spinal cord

“…2B). These results support the hy- Chen et al, 1999). Most of these cells are primary dopaminergic neurons (Binor and Heathcote, 2001).…”