Reduced sleep and impaired sleep initiation in adult male rats exposed to alcohol during early postnatal period.
ABSTRACT Prenatal alcohol exposure (AE) is associated with cognitive and neurobehavioral abnormalities, such as increased motor activity and elevated anxiety, that may last a lifetime. Persistent sleep disruption may underlie these problems. Using a rat model, we investigated long-term alterations of sleep-wake behavior following AE during a critical early developmental period. Male rats received 2.6 g/kg of alcohol intragastrically twice daily on postnatal days (PD) 4-9, a developmental period equivalent to the third trimester of human pregnancy (AE group), or were sham-intubated (S group). On PD52-80, they were instrumented for tethered electroencephalogram and nuchal electromyogram recording and habituated to the recording procedures. Sleep-wake behavior was then recorded during one 24 h-long session. Wake, slow-wave sleep (SWS) and rapid eye movement sleep (REMS) were scored in 10 s epochs during 6h of the lights-on (rest) and 6h of the lights-off (active) periods. During the active period, REMS percentage was significantly lower (4.7 ± 0.9 (SE) vs. 8.2 ± 0.9; p < 0.02) and the percentage of SWS tended to be lower (p = 0.07) in AE than S rats (N = 6/group). During the rest period, sleep and wake amounts did not differ between the groups, but AE rats had longer latency to both SWS and REMS onset (p = 0.02 and 0.003, respectively). Our data demonstrate that, in a rat model of prenatal AE, impaired sleep-wake behavior persists into the adulthood. Disordered sleep may exacerbate cognitive and behavioral disorders seen in human victims of prenatal AE.
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ABSTRACT: Perinatal Alcohol exposure (AE) has multiple detrimental effects on cognitive and various behavioral outcomes, but little is known about its impact on the autonomic functions. In a rat model of fetal alcohol spectrum disorders (FASD), we investigated neurochemical and neuroanatomical alterations in two brainstem nuclei, the hypoglossal nucleus (XIIn) and the dorsal nucleus of the vagus nerve (Xdn). One group of male Sprague-Dawley rats (n=6) received 2.625g/kg ethanol intragastrically twice daily on postnatal days (PD)4-9, a period equivalent to the third trimester of human pregnancy, and another group (n=6) was sham-intubated. On PD18-19, the rats were perfused and medullary sections were immunohistochemically processed for choline acetyltransferase (ChAT) or two aminergic receptors that mediate excitatory drive to motoneurons, α1-adrenergic (α1-R) and serotonin 2A (5-HT2A-R), and c-Fos. Based on ChAT labeling, AE rats had reduced numbers of motoneurons in the ventral XIIn (XIIn-v; 35.4±1.3 motoneurons per side and section vs. 40.0±1.2, p=0.022), but not in the dorsal XIIn or Xdn. Consistent with ChAT data, both the numbers of α1-R-labeled motoneurons in the XIIn-v and the area of the XIIn-v measured using 5-HT2A-R staining were significantly smaller in AE rats (19.7±1.5 vs. 25.0±1.4, p=0.031 and 0.063 mm(2) ±0.002 vs. 0.074±0.002, p=0.002, respectively). Concurrently, both 5-HT2A-R and c-Fos staining tended to be higher in AE rats, suggesting an increased activation. Thus, postnatal AE causes motoneuronal loss in the XIIn-v. This may compromise upper airway control and contribute to increased risk of upper airway obstructions and sudden infant death in FASD victims.Journal of chemical neuroanatomy 08/2013; · 1.75 Impact Factor