Developmental differences in cortical and hippocampal vulnerability to intermittent hypoxia in the rat

Obstructive sleep apnea is characterized by intermittent hypoxic events dur ing sleep, and is associated with substantial neurocognitive morbidity, par ticularly in children. Intermittent hypoxia (IH) leads to increases in apop tosis in the cortex and hippocampus of the adult rat, peaking at 48 h of ex posure. To examine whether the susceptibility to IH exhibits developmental differences, rats were exposed to 48 h of IH at ages 2, 5, 10, 15, 20, 25, 30, 60, and 120-day postnatally, and apoptosis was determined by terminal d eoxy-nucleotidyl transferase-mediated in situ end labeling and immunohistoc hemical staining for single-stranded DNA. Although IH induced apoptosis at all postnatal ages, smaller increases were apparent in 2 and 5-day old (P < 0.01 vs. any other age) while peak apoptosis occurred at 10-25 days (P < 0 .001 vs. 30, 60, and 120 days). We conclude that a unique window of vulnera bility to IH is present in the cortex and hippocampus during post-natal mat uration, and may underlie the high frequency of neurobehavioral deficits as sociated with obstructive sleep apnea in children. (C) 2001 Elsevier Scienc e Ireland Ltd. All rights reserved.