Effects of co-exposure to 900 MHz radiofrequency electromagnetic fields and high-level noise on sleep, weight, and food intake parameters in juvenile rats.

OBJECTIVE: Electrohypersensitive people attribute various symptoms to exposure of radiofrequency electromagnetic fields (RF-EMF); sleep disturbance is the most frequently cited. However, laboratory experiments have yielded conflicting results regarding sleep alterations. Our hypothesis was that exposure to RF-EMF alone would lead to slight or non-significant effects but that co-exposure to RF-EMFs and other environmental constraints (such as noise) would lead to significant effects. METHODS: 3-week-old male Wistar rats (4 groups, n = 12 per group) were exposed for 5 weeks to continuous RF-EMF (900 MHz, 1.8 V/m, SAR = 30 mW/kg) in the presence or absence of high-level noise (87.5 dB, 50-20000 Hz) during the rest period. After 5 weeks of exposure, sleep (24 h recording), food and water intakes, and body weight were recorded with or without RF-EMF and/or noise. At the end of this recording period, sleep was scored during the 1 h resttime in the absence of noise and of RF-EMF exposure. RESULTS: Exposure to RF-EMF and/or noise was associated with body weight gain, with hyperphagia in the noise-only and RF-EMF + noise groups and hypophagia in the RF-EMF-only group. Sleep parameters recording over 24 h highlighted a higher frequency of active wakefulness in the RF-EMF-only group and a lower non-rapid eye movement/rapid eye movement sleep ratio during the active period in the noise-only group. There were no differences in sleep duration in either group. During the 1-h, constraint-free sleep recording, sleep rebound was observed in the noise-only group but not in the RF-EMF-only and RF-EMF + noise groups. CONCLUSION: Our study showed effects of RF-EMF, regardless of whether or not the animals were also exposed to noise. However, the RF-EMF + noise group presented no exacerbation of those effects. Our results did not support the hypothesis whereby the effects of RF-EMF on physiological functions studied are only visible in animals exposed to both noise and RF-EMF.

c-Fos expression in the limbic thalamus following thermoregulatory and wake-sleep changes in the rat.

A cellular degeneration of two thalamic nuclei belonging to the "limbic thalamus", i.e., the anteroventral (AV) and mediodorsal (MD) nuclei, has been shown in patients suffering from Fatal Familial Insomnia (FFI), a lethal prion disease characterized by autonomic activation and severe insomnia. To better assess the physiological role of these nuclei in autonomic and sleep regulation, c-Fos expression was measured in rats during a prolonged exposure to low ambient temperature (Ta, - 10 °C) and in the first hours of the subsequent recovery period at normal laboratory Ta (25 °C). Under this protocol, the thermoregulatory and autonomic activation led to a tonic increase in waking and to a reciprocal depression in sleep occurrence, which was more evident for REM sleep. These effects were followed by a clear REM sleep rebound and by a rebound of Delta power during non-REM sleep in the following recovery period. In the anterior thalamic nuclei, c-Fos expression was (1) larger during the activity rather than the rest period in the baseline; (2) clamped at a level in-between the normal daily variation during cold exposure; (3) not significantly affected during the recovery period in comparison to the time-matched baseline. No significant changes were observed in either the MD or the paraventricular thalamic nucleus, which is also part of the limbic thalamus. The observed changes in the activity of the anterior thalamic nuclei appear, therefore, to be more specifically related to behavioral activation than to autonomic or sleep regulation.

Thermoregulatory correlates of nausea in rats and musk shrews.

Nausea is a prominent symptom and major cause of complaint for patients receiving anticancer chemo- or radiation therapy. The arsenal of anti-nausea drugs is limited, and their efficacy is questionable. Currently, the development of new compounds with anti-nausea activity is hampered by the lack of physiological correlates of nausea. Physiological correlates are needed because common laboratory rodents lack the vomiting reflex. Furthermore, nausea does not always lead to vomiting. Here, we report the results of studies conducted in four research centers to investigate whether nausea is associated with any specific thermoregulatory symptoms. Two species were studied: the laboratory rat, which has no vomiting reflex, and the house musk shrew (Suncus murinus), which does have a vomiting reflex. In rats, motion sickness was induced by rotating them in their individual cages in the horizontal plane (0.75 Hz, 40 min) and confirmed by reduced food consumption at the onset of dark (active) phase. In 100% of rats tested at three centers, post-rotational sickness was associated with marked (~1.5°C) hypothermia, which was associated with a short-lasting tail-skin vasodilation (skin temperature increased by ~4°C). Pretreatment with ondansetron, a serotonin 5-HT3 receptor antagonist, which is used to treat nausea in patients in chemo- or radiation therapy, attenuated hypothermia by ~30%. In shrews, motion sickness was induced by a cyclical back-and-forth motion (4 cm, 1 Hz, 15 min) and confirmed by the presence of retching and vomiting. In this model, sickness was also accompanied by marked hypothermia (~2°C). Like in rats, the hypothermic response was preceded by transient tail-skin vasodilation. In conclusion, motion sickness is accompanied by hypothermia that involves both autonomic and thermoeffector mechanisms: tail-skin vasodilation and possibly reduction of the interscapular brown adipose tissue activity. These thermoregulatory symptoms may serve as physiological correlates of nausea.