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To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol ([E.sub.2]) replacement on c-Fos immunoreactivity in sleep/ wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 17[beta]-[E.sub.2] (10.5 [micro]g; to mimic diestrous [E.sub.2] levels) or oil. After 2 wk, animals with [E.sub.2] capsules received a single subcutaneous injection of 17[beta]-[E.sub.2] (10 [micro]g/kg; to achieve proestrous [E.sub.2] levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by 'gentle handling' for 6 h during the early light phase, and killed. [E.sub.2] treatment increased serum [E.sub.2] levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousal-promoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high [E.sub.2] treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high [E.sub.2] treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that [E.sub.2] replacement modulates SD-induced or spontaneous c-Fos expression in sleep/wake-regulatory and limbic forebrain nuclei. These modulatory effects of [E.sub.2] replacement on neuronal activity may be, in part, responsible for [E.sub.2]'s influence on sleep/wake behavior. ovariectomy; immunohistochemistry: orexin/hypocretin; tuberomammillary nucleus; ventrolateral preoptic nucleus

Deurveilher S, Cumyn EM, Peers T, Rusak B, Semba K. Estradiol replacement enhances sleep deprivation-induced c-Fos immunoreactivity in forebrain arousal regions of ovariectomized rats. Am J Physiol Regul Integr Comp Physiol 295: RI 328-RI 340, 2008. First published August 27, 2008; doi: 10.1 152/ajpregu.90576.2008.-To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol (E[sub2]) replacement on c-Fos immunoreactivity in sleep! wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 1713-E[sub2] (10.5 μg; to mimic diestrous E[sub2] levels) or oil. After 2 wk, animals with E[sub2] capsules received a single subcutaneous injection of 17β-E[sub2] (10 μg/kg; to achieve proestrous E[sub2] levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by "gentle handling" for 6 h during the early light phase, and killed. E[sub2] treatment increased serum E[sub2] levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousalpromoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high E[sub2] treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high E[sub2] treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that E[sub2] replacement modulates SD-induced or spontaneous c-Fos expression in sleep!wake-regulatory and limbic forebrain nuclei. These modulatory effects of E[sub2] replacement on neuronal activity may be, in part, responsible for E[sub2]'s influence on sleep!wake behavior. [ABSTRACT FROM AUTHOR]

Light exposure at night causes an acute increase in human body temperature, which normally falls during the night. This change is largely attributable to the suppression by light of the nocturnal rise in melatonin levels. Little is known, however, about the effects of light on body temperature in nocturnally active mammals in which the nightly peak in melatonin secretion coincides with the circadian phase of elevated, rather than decreased, body temperature. We investigated the effects of a 1-h exposure to light on body temperature and activity of Syrian hamsters, Mesocricetus auratus, at two phases during the night and at two phases during the projected day. Brain or abdominal temperature was recorded continuously using implanted radio transmitters while locomotor activity was monitored simultaneously using a passive infrared movement detector. Responses to light exposure were strongly circadian phase dependent; light during the night caused elevations in both brain and core body temperature, whereas light during the projected day did not. Temperature increases at night could not be attributed solely to activity increases at the onset of light pulses, indicating a contribution from nonbehavioral mechanisms of thermogenesis. These results provide the first evidence for circadian modulation of acute temperature responses to light in a nocturnal mammal.