Co-sleeping proponents consider the practice to be "natural" and a potential protection against sudden infant death syndrome (SIDS); others consider the practice of an infant sleeping in the parents' bed for prolonged periods at night to place an infant at risk for harm or death. For this study, co-sleeping was investigated from a different perspective, that is, as a significant early experience to investigate as it may have implications for the infant's development. The sleep of 101 normal, full-term infants was recorded nonintrusively in the home for 24 hr periods when they were 5 weeks and 6 months old. Infants were assigned to three groups: short-term co-sleepers, long-term co-sleepers, and non-co-sleepers. Their sleep states and wakefulness were compared at the two ages and over age. At 5 weeks and 6 months, the long-term co-sleeping infants differed significantly from the non-co-sleepers on a number of measures: At 5 weeks, they showed more quiet sleep and longer bouts of quiet sleep; and at 6 months, they also showed less active sleep, fewer arousals in active sleep, and less wakefulness. Each of these differences indicates a markedly lower arousal level in the long-term co-sleeping infants. This sleep pattern has been repeatedly found to be an indicator of stress. We infer that a major source of stress for these infants is the experience of sleep disturbance documented for infants when they were co-sleeping. Based on extensive evidence for long-term effects of early stress, we conclude that co-sleeping should have significant implications for infants' neurobehavioral development.
We investigated the interaction between norepinephrine (NE) and orexin/hypocretin (Hcrt) in the control of sleep behavior and narcoleptic symptoms by creating mice that were deficient in both neurotransmitters. Mice with a targeted disruption of the dopamine b-hydroxylase (Dbh) gene (deficient in NE and epinephrine) or the Hcrt gene were bred to generate double knockouts (DKOs), each single KO (Dbh-KO and Hcrt-KO), and control mice. The duration of wake, non-rapid eye movement (NREM) and REM sleep were monitored by electroencephalogram (EEG)/electromyogram (EMG) recording over a 24-h period, and the occurrence of behavioral arrests was monitored by video/EEG recording for 4 h. Overall, there was very little interaction between the two genes; for most parameters that were measured, the DKO mice resembled either Dbh-KO or Hcrt-KO mice. REM sleep was increased in both DKO and Hcrt-KO mice at night relative to the other groups, but DKO mice had significantly more REM sleep during the day than the other three groups. Sleep latency in response to saline or amphetamine injections was reduced in Dbh-KO and DKO mice relative to other groups. Behavioral arrests, that are frequent in Hcrt-KO mice, were not exacerbated in DKO mice.
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