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Journal of Neuroscience, Vol 10, 2156-2175, Copyright © 1990 by Society for Neuroscience
Axon overproduction and elimination in the corpus callosum of the developing rhesus monkey
AS LaMantia and P Rakic
Section of Neuroanatomy, Yale University School of Medicine, New Haven, Connecticut 06510.
We have studied the cytological and quantitative aspects of axon addition
and elimination in the corpus callosum of the developing rhesus monkey.
Electron microscopic analysis reveals that during fetal development the
number of callosal axons increases from 4 million at embryonic day 65 (E65)
to 188 million at birth (E 165). Thus, the number of callosal axons in
newborn monkeys exceeds the number present in the adult (an average of 56
million; LaMantia and Rakic, 1990a) by at least 3.5 times. Although there
is some variability among the 11 fetal and newborn monkeys examined, there
appears to be a progressive increase in the total number of callosal axons
from midgestation through birth. The presence and numbers of growth cones
from E65 through birth suggests that axon addition occurs exclusively
during this period. There is no ultrastructural or quantitative indication
of postnatal axon addition. After birth, about 70% of the axons in the
callosum are eliminated in 2 phases. During the first phase, which includes
the first 3 postnatal weeks, approximately 80 million axons are lost at an
estimated rate of 4.4 million/d or 50/sec. During the second phase, which
continues for the following 3 months, an additional 50 million axons are
eliminated at a rate of 0.5 million/d or 5/sec until the adult value is
reached. A discontinuous distribution of different classes of axons along
the anterior-posterior axis of the tract reminiscent of the pattern seen in
the adult is detectable before the onset of the first phase of axon
elimination. Since the basic topography and terminal field patterns of
callosal projections are well established before birth in all regions of
the monkey cortex examined so far (Goldman-Rakic et al., 1983; Killackey
and Chalupa, 1986; Dehay et al., 1988; Schwartz and Goldman-Rakic, 1990),
we conclude that the massive postnatal elimination of callosal axons
described here is unlikely to play a significant role in the development of
discretely patterned callosal projection zones or their columnar
terminations. The coincidence of axon elimination and the increase in
synaptic density throughout the primate cerebral cortex during the first 6
postnatal months (Rakic et al., 1986), however, suggests that supernumerary
axons may be lost during a process that results in the local proliferation
of synapses from a subset of initial interhemispheric projections.
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