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Biomedical subjects

Allan I Pack

Publications and source records attributed to Allan I Pack.

39 records · Page 3Linked to original sources

Brain glycogen decreases with increased periods of wakefulness: implications for homeostatic drive to sleep.

Sleep is thought to be restorative in function, but what is restored during sleep is unclear. Here we tested the hypothesis that increased periods of wakefulness will result in decreased levels of glycogen, the principal energy store in brain, and with recovery sleep levels of glycogen will be replenished, thus representing a homeostatic component of sleep drive. Using a high-energy focused microwave irradiation method to kill animals and thereby snap-inactivate glycogen-producing and -metabolizing enzymes, we determined, with accuracy and precision, levels of brain glycogen and showed these levels to decrease significantly by approximately 40% in brains of rats deprived of sleep for 12 or 24 hr. Recovery sleep of 15 hr duration after 12 hr of sleep deprivation reversed the decreases in glycogen. Using a novel histochemical method to stain brain glycogen, we found glycogen to be concentrated in white matter; this finding was confirmed biochemically in white matter dissected from rats killed with microwave irradiation. Levels of glycogen, as determined histochemically, were significantly decreased in gray and white matter with sleep deprivation, and these decreases were reversed with recovery sleep. The observed decreases in levels of brain glycogen may be a consequence of increased wakefulness and/or a component integral to the homeostatic drive to sleep.

Animals↗

Linear dimensions of the upper airway structure during development: assessment by magnetic resonance imaging.

The upper airway undergoes progressive changes during childhood. Using magnetic resonance imaging (MRI), we studied the growth relationships of the tissues surrounding the upper airway (bone and soft tissues) in 92 normal children (47% males; range, 1 to 11 yr) who underwent brain MRI. None had symptoms of sleep-disordered breathing or conditions that impacted on their upper airway. MRI was performed under sedation. Sequential T1-weighted spin echo sagittal and axial sections were obtained and analyzed on a computer. We measured lower face skeletal growth along the midsagittal and axial oropharyngeal planes. In the midsagittal plane the mental spine-clivus distance related linearly to age (r = 0.86, p < 0.001). Along this axis, the dimensions of tongue, soft palate, nasopharyngeal airway, and adenoid increased with age and maintained constant proportion to the mental spine-clivus distance. Similarly, a linear relationship was noted for mandibular growth measured along the intermandibular line on the axial plane and age (r = 0.78, p < 0.001). In addition, the intertonsillar, tonsils, parapharyngeal fat pads, and pterygoids widths maintained constant proportion to intermandibular width with age. We conclude that the lower face skeleton grows linearly along the sagittal and axial planes from the first to the eleventh year. Our data indicate that soft tissues, including tonsils and adenoid, surrounding the upper airway grow proportionally to the skeletal structures during the same time period.

Adenoids↗

Sleep deprivation selectively impairs memory consolidation for contextual fear conditioning.

Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0-5 and 5-10 h after training for contextual and cued fear conditioning. We found that sleep deprivation from 0-5 h after training for this task impaired memory consolidation for contextual fear conditioning whereas sleep deprivation from 5-10 h after training had no effect. Sleep deprivation at either time point had no effect on cued fear conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for fear conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage.

Analysis of Variance↗