Effects of short nap and exercise on elderly people having difficulty in sleeping.

The purpose of the present study was to examine the effects of short nap and exercise on the sleep quality of elderly people who reported difficulty in sleeping. 'Interventions' such as short nap after lunch and moderate-intensity exercise in the evening were carried out for 4 weeks. After the 'interventions', wake time after sleep onset significantly decreased and sleep efficiency significantly increased, which showed that sleep quality was improved. The frequency of nodding in the evening significantly decreased. These results demonstrated that the proper awakening maintenance in the evening was effective in improving sleep quality. After the 'intervention', mental health was also improved with improving sleep quality.

A survey of junior high school students' sleep habit and lifestyle in Okinawa.

A survey was made of the sleep and lifestyle activity patterns of 3754 students from 14 different junior high schools on Okinawa Island. The survey showed that bedtimes became progressively and significantly later as students ascended to higher grades, resulting in adolescent sleep debt. The later adolescents retired to sleep, there appeared significantly greater numbers suffering from insufficient sleep, who found difficulty in waking up, who arose later in the mornings, and who failed to eat breakfast. The study indicated that along with later bedtimes, staying up late resulted in deterioration of sleep health, poor dietary habits and feeling ill, contributing to sleepiness during class.

Survey of sleep-health and lifestyle of the elderly in Okinawa.

A total of 788 people (aged from 60 to 93 years) living in the Okinawa prefecture, renowned for the long life expectancy of its citizens, were randomly chosen as subjects. A questionnaire based on lifestyle and sleep-health was distributed. Following this, subjects were chosen in groups of nine from the good sleep-health group and then from the poor sleep-health group based on the results of the survey; their physical activities were then recorded using actigraphs for 1 week. This study suggested that lifestyle, such as exercise, walking and short naps, occupies an important position in the maintenance and improvement of sleep-health. It also verified the reliability of the sleep-health risk index and the questionnaire.

Effects of Hemerocallis on sleep in mice.

Freeze-dried flowers of the Akinowasuregusa (Hemerocallis fulva L. var. sempervirona M. Hotta), a Hemerocallis genus of the lily family, were fed to C57BL strain mice. The slow wave sleep and paradoxical sleep of the Hemerocallis-treated group increased during the dark period. The differences between the control group and the Hemerocallis-treated group were significant (P < 0.05). The Hemerocallis feeding did not cause a change in sleep time during the light period. As a result, there was no significant change in the sleep-time percentage over a 24-h period.

Effects of dietary phosphatidylcholine on memory in memory deficient mice with low brain acetylcholine concentration.

Data concerning the effect of phosphatidylcholine (PCh) administration on the improvement of memory in senile dementia of Alzheimer type are inconsistent, probably due to the different conditions under which studies were conducted. Animal studies provide a good model, but data on this is limited. We studied the effect of PCh on memory in memory deficient mice (Dull mice) with low brain acetylcholine (ACh) concentration and normal mice. Mice were fed 24% casein diet (control) or this diet supplemented with 2 or 8% egg yolk PCh from gestation (Experiment 1) and after weaning (Experiment 2). Memory acquisition and retention were studied by step-down type passive avoidance performance at 8 and 10 weeks old, respectively. Control group of Dull mice had poorer memories than that of the normal mice in Experiments 1 and 2. On the 2% PCh diet, Dull mice improved memory acquisition and retention in Experiment 1 and retention in Experiment 2. On the 8% PCh diet in Dull mice there was improvement of memory and retention in Experiment 1, but no effect was observed in Experiment 2 (P > 0.05). In the normal mice, the 2% PCh diet did not affect memory acquisition and retention, however on the 8% PCh diet, there was no or adverse effect. These results suggest that dietary supplementation of egg yolk PCh improves memory of Dull mice, particularly when given from gestation and that the 2% PCh diet elicits better response than the 8% PCh diet.

Effects of dietary nucleoside-nucleotide mixture on memory in aged and young memory deficient mice.

Intestinal mucosa, bone marrow hematopoietic cells and brain have limited capacity for the de novo synthesis of nucleosides (NSs) and nucleotides (NTs). Whereas the role of dietary NS and NT in the former two tissues is known, it is not known in the brain. Therefore we studied the effect of dietary NS and NT mixture on memory in aged mice (Experiment 1) and young memory deficient mice (Experiment 2). Memory retention was studied by step-through type passive avoidance performance (maximum 180 seconds). In Experiment 1 aged (7 month old) senescence accelerated mice (SAM) were fed 20% casein diet (control) or this diet supplemented with 0.5% NS/NT mixture for 12 weeks. Memory was studied 1, 2 and 3 days after the electric shock (punishment). In Experiment 2, young (1 month old) memory deficient mice (Dull mice) and normal mice (ddY mice) were fed the same diets as those in Experiment 1 for 12 weeks. Memory retention was studied 1 and 3 days after the punishment. In the aged SAM the average time of avoidance and also the percentages of successful memory 2 and 3 days after the punishment were significantly higher in the NS/NT diet group than the control diet group (P < 0.05). In the Dull mice percentage of successful memory was higher in the NS/NT diet group than in the control group 3 days after the punishment, however, such an effect was not observed in the normal mice. These results suggest that insufficient endogenous supply of NSs and NTs may be responsible for the factor of memory deficiency with aging or of genetical memory deficiency, which can be improved by the dietary administration of NSs and NTs.

Administration of phosphatidylcholine increases brain acetylcholine concentration and improves memory in mice with dementia.

Studies on the effect of phosphatidylcholine administration on memory are limited. We administered egg phosphatidylcholine to mice with dementia and to normal mice and compared the differences in memory and serum choline concentration, and choline and acetylcholine concentrations and choline acetyltransferase activities of three forebrain regions (cortex, hippocampus and the remaining forebrain). Mice with dementia were produced by mating sibling mice who had impaired memory for > 20 generations. These mice had poor memory and low brain acetylcholine concentration. We administered 100 mg of egg phosphatidylcholine (phosphatidylcholine group) or water (control group) by gavage to each mouse daily for about 45 d. Control mice with dementia had poorer memory in passive avoidance performance and lower brain choline (cortex and hippocampus) and acetylcholine (hippocampus and forebrain excluding cortex and hippocampus) concentrations and lower cortex choline acetyltransferase activity than the control normal mice (P < 0.05). The administration of phosphatidylcholine to mice with dementia improved memory and generally increased brain choline and acetylcholine concentrations to or above the levels of the control normal mice. In normal mice, phosphatidylcholine treatment did not affect memory or acetylcholine concentrations in spite of the great increase in choline concentrations in the three brain regions. Serum choline concentration in mice treated with phosphatidylcholine increased to a similar level in both strains of mice, indicating that the absorption of phosphatidylcholine was not impaired in mice with dementia. The results suggest that administration of egg phosphatidylcholine to mice with dementia increases brain acetylcholine concentration and improves memory.

H(+)-ATPase and transport of DOPAC, HVA, and 5-HIAA in monoamine neurons.

The effects of N-methylmaleimide (N-MtM), a vacuolar H(+)-ATPase inhibitor, were evaluated in the putamen of the cat to study the in vivo transport mechanisms of dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindolacetic acid (5-HIAA), using the brain focal microdialysis technique combined with HPLC. The addition of N-MtM to the perfusate altered invariably the flux of the DOPAC, HVA, and 5-HIAA in a similar pattern, resulting in a decrease of the extracellular levels of such metabolites, its extent being N-MtM concentration dependent, thus indicating that the mechanism(s) of such a decrease is (are) related most likely to decreased transport from the intracellular to the extracellular space as the consequence of the inhibition of the vacuolar H(+)-ATPase of DA and 5-HT neurons by the N-MtM. Furthermore, N-MtM masked the release of DA and 5-HT produced by KCl 120 mmol/l. Indeed, N-MtM increased the extracellular levels of such transmitters to values exceeding 4 to 6 times of those produced by KCl 120 mmol/l alone, which suggests that vacuolar H(+)-ATPase is probably involved also in the retention and/or reuptake process of DA and 5-HT.

Active transport pumps of HVA and DOPAC in dopaminergic nerve terminals.

The effect of the membrane potential on the efflux of HVA and DOPAC from DA neurons was studied in anesthetized (1% halothane in gas mixture of 70% N2O and 30% O2) cats. Extracellular DA, HVA and DOPAC were measured continuously from the putamen, the hypothalamus, the thalamus, the raphe nuclei and the cortex using brain microdialysis technique combined with HPLC-ED monoamine measurements. HVA and DOPAC concentrations were highest in the putamen and lowest in the cerebral cortex. Extracellular HVA levels exceed those of the DOPAC. Increases in the extracellular potassium from 4 to 120 mM invariably produced decreases of the extracellular HVA and DOPAC in all the tested brain regions. These decreases were inversely proportional to the extracellular potassium concentration. Thus, it is concluded that the HVA and the DOPAC are extruded from inside the cell to the extracellular space by active mechanisms of transport similar to that reported for 5-HIAA in serotonergic neurons.

Efflux of 5-HIAA from 5-HT neurons: a membrane potential-dependent process.

The effect of the membrane potential on the efflux of 5-HIAA from 5-HT neurons was studied in anesthetized (halothane: 1% in gas mixture of N2O: 70% and O2: 30%) cats. The endogenous 5-HT and its metabolite 5-HIAA were measured continuously from the cortex, the thalamus, the hypothalamus and the raphe nuclei using brain microdialysis technique combined with HPLC-ED monoamine measurements. Membrane potential variations were induced by changing the extracellular concentration of potassium through the microdialysis membrane. The levels of the extracellular 5-HIAA varied according to the different regions of the brain, being highest in the hypothalamus and lowest in the cerebral cortex. Increases in the extracellular potassium from 4 to 120 mM invariably produced a decrease of the extracellular 5-HIAA in all the tested brain regions. This decrease was inversely proportional to the logarithm of extracellular potassium concentration. Thus, it is postulated that the 5-HIAA is moved from inside the cell to extracellular space by an active mechanism of transport electrically coupled to the membrane potential.

Time-dependent effects of actinomycin S3 on sleep and brain concentrations of 5-hydroxytryptamine in the rat.

Changes in the sleep pattern were investigated in rats given actinomycin S3 (AcS3, 0.25 mg/kg, intraventricularly), an inhibitor of RNA synthesis, at 0000, 0600, 1200, and 1800. The amounts of slow-wave (SS) and paradoxical sleep (PS) were increased during the dark period (1800 to 0600) in the groups treated at 0000, 0600, and 1200. In the 1800 injected group, PS was decreased. 5-Hydroxytryptamine (5-HT) was determined in the 0600 injected group. The 5-HT concentration in the AcS3-treated group was twofold higher than in the control group at 1800 (12 h after administration) in the cerebral cortex and lower brain stem but returned to control values at 0000 (18 h after) while sleep time continued to increase. Thus, AcS3 affected the circadian rhythm of the sleep-wake cycle. The increase of sleep time in the dark period was independent of changes in brain 5-HT content.

Reversible depression of spontaneous brain electrical activity induced by actinomycin D and 7-aminoactinomycin D in rats.

Various types of actinomycin (C,D,S2, I and V) and 7-amino-analogue of actinomycin D were injected into the right lateral ventricle of the brain through a chronically implanted cannula. In rats but not in mice actinomycin D, actinomycin S2 and 7-aminoactinomycin D caused depression of EEG, while cardiac and respiratory activity were maintained. This effect of the EEG was reversible and a normal EEG pattern reappeared at least 3 h after administration.

Spindle-like activity appearing during paradoxical sleep in rats with iron-induced cortical focus.

Under barbiturate anesthesia, male Wistar rats weighing 250-300 g were injected with 2.5 microliters of 0.2 M FeCl3 solution into the left sensori-motor cortex to induce an epileptic focus with minimal abnormal activities. Polygraphy started 1 week after the surgery, showed a spindle-like hypersynchronous activity that appeared not only in the slow wave sleep period but also during paradoxical sleep (PS). This activity had a frequency of 8-14 Hz. The amplitude was more than 200 mu v in the right (non-injected side) cortex but very small in the left cortex (injected side). Isolated spike discharges were observed in an ECoG of slow wave sleep. Apart from this activity there was nothing resembling the usual sleep spindles.

Change in somatosensory evoked potential in the rat recorded at the hemisphere with iron-induced epileptic focus.

In rats, microinjection of FeCl3 solution into the left sensorimotor cortex was performed to induce a chronic epileptic focus. One month or more after the microinjection, electrocutaneous stimuli were applied to part of the wrist joint and 50 consecutive somatosensory evoked potentials (SEPs) were averaged. SEP from the left cortex showed only an initial negative monophasic deflection while SEP from the contralateral cortex showed a normal configuration with initial positive-negative biphasic deflection in the majority of experimental animals.