[S31]: Signal transduction mechanisms in axon guidance

development of new behavioral deficits over time. There may also be secondary structural consequences of cell death during development: examples include abnormal cortical patterning at the edges of an infarct in developing cortex, and long term deficiencies in myelination after death of oligodendrocyte precursors. The results of experimental studies with relatively short term survival periods may thus, not correlate with longterm outcome. Effects of resuscitation and treatment: Infants with hypoxia or ischemia are commonly treated with 100% oxygen. Particularly in the premature infant, oxygen may exacerbate brain injury, as in the retina and lung. For any proposed treatment, the effects on normal developmental processes must be considered. While excitotoxicity is a major mechanism of neuronal injury, inhibition of excitatory neurotransmitters may have deleterious effects on normal brain development. Similarly, certain cytokines that are considered to promote cell death also have normal expression in brain development. The functions of many molecules change significantly, sometimes diametrically, during development.