Prenatal intermittent hypoxia sensitizes the laryngeal chemoreflex, blocks serotoninergic shortening of the reflex, and reduces 5-HT3 receptor binding in the NTS in anesthetized rat pups.

We tested the hypothesis that exposure to intermittent hypoxia (IH) during pregnancy would prolong the laryngeal chemoreflex (LCR) and diminish the capacity of serotonin (5-hydroxytryptamine; 5-HT) to terminate the LCR. Prenatal exposure to IH was associated with significant prolongation of the LCR in younger, anesthetized, postnatal day (P) rat pups age P8 to P16 compared to control, room air (RA)-exposed rat pups of the same age. Serotonin microinjected into the NTS shortened the LCR in rat pups exposed to RA during gestation, but 5-HT failed to shorten the LCR in rat pups exposed to prenatal IH. Given these observations, we tested the hypothesis that prenatal hypoxia would decrease binding to 5-HT3 receptors in the nucleus of the solitary tract (NTS) where 5-HT acts to shorten the LCR. Serotonin 3 receptor binding was reduced in younger rat pups exposed to IH compared to control, RA-exposed rat pups in the age range P8 to P12. Serotonin 3 receptor binding was similar in older animals (P18-P24) regardless of gas exposure during gestation. The failure of the 5-HT injected into the NTS to shorten the LCR was correlated with a developmental decrease in 5-HT3 receptor binding in the NTS associated with exposure to prenatal IH. In summary, prenatal IH sensitized reflex apnea and blunted processes that terminate reflex apneas in neonatal rat pups, processes that are essential to prevent death following apneas such as those seen in babies who died of SIDS.

The Lateral Temporal Lobe in Early Human Life.

Abnormalities of lateral temporal lobe development are associated with a spectrum of genetic and environmental pathologic processes, but more normative data are needed for a better understanding of gyrification in this brain region. Here, we begin to establish guidelines for the analysis of the lateral temporal lobe in humans in early life. We present quantitative methods for measuring gyrification at autopsy using photographs of the gross brain and simple computer-based quantitative tools in a cohort of 28 brains ranging in age from 27 to 70 postconceptional weeks (end of infancy). We provide normative ranges for different indices of gyrification and identify a constellation of qualitative features that should also be considered in these analyses. The ratio of the temporal area to the whole brain area increased dramatically in the second half of gestation, but then decelerated after birth before increasing linearly around 50 postconceptional weeks. Tertiary gyrification continued beyond birth in a linear process through infancy with considerable variation in patterns. Analysis of 2 brains with gyral disorders of the lateral temporal lobe demonstrated proof-of-principle that the proposed methods are of diagnostic value. These guidelines are proposed for assessments of temporal lobe pathology in pediatric brains in early life.