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Mechanisms of Hypoxic Neurodegeneration in the Developing Brain
Michael V. Johnston
Kennedy Krieger Institute, 707 North Broadway, Baltimore, MD 21205; Johnston{at}kennedykrieger.org
Wako Nakajima
Henrik Hagberg
Asphyxia and other insults to the developing brain are responsible for several human neurodevelopmental disorders. The pattern of neonatal brain injury differs from that seen in the adult nervous system, and there are wide differences in regional vulnerability. Recent evidence suggests that two events that contribute to this pattern of selective vulnerability are developmental changes in excitatory glutamate-containing neurotransmitter circuits and the propensity for immature neurons to die by apoptosis rather than necrosis. Developmental up-regulation of NMDA receptors with enhanced function and increased expression of caspase-3 at critical periods in development are linked to these mechanisms. Although these molecular changes enhance the developing brain's capacity for plasticity by helping to prune redundant synapses and neurons, they can become "Achilles heels" in the face of a brain energy crisis.
Key Words: Hypoxia • Caspase • Neonate • Glutamate • NMDA
The Neuroscientist, Vol. 8, No. 3,
212-220 (2002)
DOI: 10.1177/1073858402008003007
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