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Introduction Our previous electrophysiologic data have provided compelling evidence that GABAergic processes in the nucleus pontis oralis (NPO) play a critical role in the generation and maintenance of wakefulness as well as active (REM) sleep (AS). We therefore hypothesized that one of the neuronal mechanisms of GABA actions in the NPO to promote wakefulness and suppress AS is due to a direct GABAergic inhibition of NPO neurons that generate AS (AS-generator neurons). However, the anatomical substrate for this inhibition is undetermined. Accordingly, the present study was undertaken to examine whether there is any direct interaction between GABAergic neurons and glutamatergic AS-generator neurons in the NPO. Methods Adult cats were deeply anesthetized and perfused transcardially. The brainstem containing the NPO was removed, postfixed and cut into 15 μm coronal sections with a Reichert-Jung cryostat. The sections were incubated with a mixture of a rabbit polyclonal antibodies against glutamine and GABA following the procedure of double fluorescence immunohistochemistry. Results There was a large number of neuronal somata labeled by anti-glutamine antibody and terminals labeled by anti-GABA antibody in the NPO. These glutamine-positive neurons were medium to large, multipolar cells (> 20 μm), which resemble glutamatergic, AS-generator neurons that have been previously identified in the NPO. Specifically, majority of glutamatergic neuronal somata were closely apposed by multiple GABAergic terminals, indicating that AS-generator neurons in the NPO receive direct GABAergic inputs. Conclusion The present results demonstrate that a direct connection exists between glutamatergic AS-generator neurons and GABAergic processes in the NPO. These data provide the anatomical evidence which supports our hypothesis that the pontine GABAergic control of wakefulness and active sleep is partially mediated via GABAergic processes project to NPO AS-generator neurons that suppress the activity of these cells. Support NS092383

Objective: An investigation was made of how postnatal maturation of cardiac control can be described by linear and non-linear methods of time series analysis. Methods: Sixteen healthy and term newborns were studied during their first 6 months of life. Power spectrum analysis including total power (TP), low frequency power (LF), high frequency power (HF) and LF/HF ratio were performed on the instantaneous heart rate (IHR) time series and mean heart rate (HR) was derived. The largest Lyapunov exponent (LLE) was calculated using a modified Wolf algorithm and checked by means of the surrogate-data test. Results: There is an age dependency for the parameters LLE, HR, TP, HF, LF, LF/HF for active and LLE, HR, TP, HF, LF/HF for quiet sleep. HR is characterised by a steep increase between the 5th and 7th day. HF demonstrates a distinct development with high values around the first week and 90–180th day and low values around the 10–60th day. TP, LF and LF/HF show significantly higher values in active sleep in comparison to quiet sleep. For all ages and sleep stages, positive LLE were found, indicating sensitivity to initial conditions, a hall-mark of chaos. For the period between the 7 and 90th days of life, the LLE for active sleep took on larger values compared with the LLE of quiet sleep. Conclusions: This study shows that by linear as well as non-linear analysis one can reveal the complexity of the IHR development in humans and may gain insight into the system controlling the heart during the period considered. The positive LLE indicate that there is a non-linear component in the heart rate control. There is no “straight line” development for the parameters analysed within the first 6 months. This may result from manifold influences on the autonomic system, due to structural and functional maturation in this period of life.

Electroencephalographic (EEG) sleep studies of 25 preterm neonates with chronic lung disease (CLD) corrected to a fullterm postconceptional age were compared with recordings from two groups of neonates without CLD: a fullterm appropriate for gestational age group (9 patients) and a preterm group studied at a corrected term postconceptional age (15 patients). Electrographic/polygraphic studies were obtained using 21-channel EEG recordings. Scores were tabulated based on minute-by-minute visual analyses of sleep state, number and duration of arousals, body movements and rapid eye movements (REM). A significant reduction in the percentage of active sleep was noted in the CLD group compared to both control groups (31.15% vs. 47.01% and 52.9%, respectively). The mean percentage of indeterminate sleep was significantly increased in the study group as compared to both control groups (31.23% vs. 15.18% and 11.5%). In addition, significant differences were noted between the CLD group and the healthy preterm control group with respect to the number (0.29/minute vs. 0.13/minute) and duration (4.8 seconds vs. 2.94 seconds) of arousals as well as the total number of body movements (1.57/minute vs. 0.74/minute). These data suggest that neurophysiological organization of the immature brain, as reflected in neonatal sleep architecture and continuity measures, is adversely affected in neonates with CLD. EEG sleep architecture and continuity measures may be helpful in predicting the longitudinal outcome of infants with CLD as this group is at risk for adverse neurodevelopmental outcome.

A procedure is described for continuous monitoring of sleep states and wakefulness of infants in the home, with no intervention required for the recording. The infant's motility patterns produced by respiration and body movements are recorded from a pressure-sensitive mattress in the crib onto a single channel of a small 24-h analog recorder. In this way, signals produced by the naturally occurring states are obtained during all portions of the day when the infant is in the crib. Later, in the laboratory, the signals are analyzed by computer, using a pattern recognition program with a template-matching procedure that scores the data every 30 s for Active Sleep, Quiet Sleep, Active-Quiet Transition Sleep, Sleep-Wake Transition, and Wakefulness. Computer-scored records for 2-h recordings of 10 infants were compared with direct behavioral state observations that were made at the same time as the mattress recording. The results confirmed the validity of the computer scoring procedure, both when templates were obtained from each infant's observation and when a standard set of templates from one infant were used for scoring the data from all other subjects.

Roffwarg et al. have proposed two complementary hypotheses to account for the finding that rapid eye movement (REM), or Active, Sleep occurs in large quantities in infancy and then drops off as the organism matures. The first assumes that the immature nervous system lacks inhibitory control and that the diminution of REM sleep reflects the maturation of the CNS. The second hypothesis postulates that REM sleep also serves a functional role, namely, to stimulate the central nervous system, thereby facilitating growth and maturation. A set of deductions, derived from the second hypothesis, was tested by analyzing the sleep-wake data of 22 normal infants. These were confirmed. The key findings were that the behavioral state of Quiet Alert correlated -0.82 with the state of Active Sleep and that this correlation was independent of maturational changes in the infants.

Conjoined twins with a common heart system and circulatory system were observed during the 14th and 15th days for 11 hr. Sleep, Waking, and Quiet and Active Sleep were recorded in minute intervals. Clear independence of sleep and waking was manifest, and total independence of Quiet and Active sleep was noted.