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The Journal of Neuroscience, April 15, 2003, 23(8):3308
Selective Vulnerability of Subplate Neurons after Early Neonatal
Hypoxia-Ischemia
Patrick S.
McQuillen1,
R. Ann
Sheldon2,
Carla J.
Shatz3, and
Donna M.
Ferriero1, 2
Departments of 1 Pediatrics and
2 Neurology, University of California San Francisco Medical
Center, San Francisco, California 94143-0106, and
3 Department of Neurobiology, Harvard Medical School,
Boston, Massachusetts 02115
Neonatal hypoxia-ischemia in the preterm human leads to selective
injury to the subcortical developing white matter, which results in
periventricular leukomalacia (PVL), a condition associated with
abnormal neurodevelopment. Maturation-dependent vulnerability of late
oligodendrocyte progenitors is thought to account for the cellular
basis of this condition. A high frequency of cognitive and sensory
deficits with decreasing gestational age suggests pervasive
abnormalities of cortical development. In a neonatal rat model of
hypoxic-ischemic injury that produces the characteristic pattern of
subcortical injury associated with human PVL, selective subplate neuron
death is seen. The premature subplate neuron death occurs after
thalamic axons have reached their targets in cortex. Thus, as expected,
thalamocortical connections form normally, including patterned
connections to somatosensory cortex. However, deficits in motor
function still occur, as in babies with PVL. Subplate neuron cell death
in PVL provides another mechanism for abnormal neurodevelopment after
neonatal hypoxia-ischemia.
Key words:
periventricular leukomalacia; visual; cortex; development; premature infant; thalamocortical
Copyright © 2003 Society for Neuroscience 0270-6474/03/2383308-08$05.00/0
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