S. Homma et al., PROGRAMMED CELL-DEATH DURING THE EARLIEST STAGES OF SPINAL-CORD DEVELOPMENT IN THE CHICK-EMBRYO - A POSSIBLE MEANS OF EARLY PHENOTYPIC SELECTION, Journal of comparative neurology, 345(3), 1994, pp. 377-395
The spatiotemporal distribution of cell death in the chick embryo neur
al tube and spinal cord (brachial region) was examined between stage (
St.) 12 and 22, in plastic semithin sections. Between St. 12 and 16, t
he total number of pycnotic cells per segment was low, whereas after S
t. 16 the number of pycnotic cells was substantially increased. Betwee
n St. 17 and 19 three cell death foci or regions could be recognized.
One region, the dorsal pycnotic zone, was located in the most dorsal p
art of the spinal cord, including the neural crest, with the highest n
umber of pycnotic cells observed at St. 18. The second region, or vent
ral pycnotic zone, was located between motoneurons and the floor plate
and had the highest number of dying cells at St. 17. The third region
, the floor plate pycnotic zone, was located in the midportion of the
floor plate and had the greatest amount of cell death at St. 19. Altho
ugh low numbers of pycnotic cells were also observed in other regions
between St. 17 and 19, no pycnotic cells were found in the ventrolater
al region that gives rise to motoneurons. Ultrastructural observations
as well as data from in situ nick end labeling indicate that the pycn
otic cells observed in the neural tube die by apoptosis and that the d
ebris from the dead cells is phagocytized primarily by adjacent health
y neuroepithelial cells. Although the spatiotemporal distribution of p
ycnotic cells suggests that cell death at these early stages could pla
y a role in establishing the pioneer axonal pathway for spinal commiss
ural neurons, preliminary observations following perturbations of cell
death do not support this notion. Alternatively, early cell death may
be involved in the regulation of cellular patterning along the dorsov
entral axis of the neural tube by a kind of negative selection of spec
ific progenitor cells. (C) 1994 Wiley-Liss, Inc.