Contrasting Effects of Ibotenate Lesions of the Paraventricular Nucleus and Subparaventricular Zone on Sleep–Wake Cycle and Temperature Regulation

Lü, Jun; Zhang, Y.-H.; Chou, Tom; Gaus, Stephanie E.; Elmquist, Joel K.; Shiromani, Priyattam J.; Saper, Clifford B.

doi:10.1523/jneurosci.21-13-04864.2001

Cited by 299 publications

(232 citation statements)

References 38 publications

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“…2). The SCN sends its densest projections to other hypothalamic nuclei, including the subparaventricular zone and dorsomedial hypothalamic nucleus, which are also required for normal circadian expression of behavioural rhythms, including feeding (17)(18)(19) . In addition to receiving input from appetite circuits, the dorsomedial hypothalamic nucleus contains different populations of neurons that project to the sleep-promoting ventrolateral preoptic nucleus and the wake-promoting lateral hypothalamic area (17) .…”

Section: Entrainment Of Feeding Circuits and Peripheral Clocksmentioning

confidence: 99%

Circadian regulation of lipid metabolism

Gooley

2016

Proc. Nutr. Soc.

144

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The circadian system temporally coordinates daily rhythms in feeding behaviour and energy metabolism. The objective of the present paper is to review the mechanisms that underlie circadian regulation of lipid metabolic pathways. Circadian rhythms in behaviour and physiology are generated by master clock neurons in the suprachiasmatic nucleus (SCN). The SCN and its efferent targets in the hypothalamus integrate light and feeding signals to entrain behavioural rhythms as well as clock cells located in peripheral tissues, including the liver, adipose tissue and muscle. Circadian rhythms in gene expression are regulated at the cellular level by a molecular clock comprising a core set of clock genes/proteins. In peripheral tissues, hundreds of genes involved in lipid biosynthesis and fatty acid oxidation are rhythmically activated and repressed by clock proteins, hence providing a direct mechanism for circadian regulation of lipids. Disruption of clock gene function results in abnormal metabolic phenotypes and impaired lipid absorption, demonstrating that the circadian system is essential for normal energy metabolism. The composition and timing of meals influence diurnal regulation of metabolic pathways, with food intake during the usual rest phase associated with dysregulation of lipid metabolism. Recent studies using metabolomics and lipidomics platforms have shown that hundreds of lipid species are circadian-regulated in human plasma, including but not limited to fatty acids, TAG, glycerophospholipids, sterol lipids and sphingolipids. In future work, these lipid profiling approaches can be used to understand better the interaction between diet, mealtimes and circadian rhythms on lipid metabolism and risk for obesity and metabolic diseases.

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Section: Entrainment Of Feeding Circuits and Peripheral Clocksmentioning

confidence: 99%

Circadian regulation of lipid metabolism

Gooley

2016

Proc. Nutr. Soc.

144

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“…The surgery and EEG/EMG data collection and analyses have been described in detail previously (Lu et al, 2000(Lu et al, , 2001. Briefly, animals were anesthetized with chloral hydrate (7% in saline, 350 mg/kg), and four stainless-steel EEG screw electrodes were implanted into the skull, in the frontal (two) and parietal (two) bones, and two flexible EMG wire electrodes were placed in the nuchal muscles.…”

Section: Eeg/emg and Sleep Recordingmentioning

confidence: 99%

“…Animals were allowed to recover from surgery for at least 1 week, including 2 days of adaptation to the EEG/EMG cables before recording. Wakefulness, NREM sleep, and REM sleep were scored as previously described in 12-second epochs (Lu et al, 2000(Lu et al, , 2001. Percentages of sleep and wake states per hour were calculated based on scored results of EEG/EMG.…”

Section: Eeg/emg and Sleep Recordingmentioning

confidence: 99%

Role of endogenous sleep‐wake and analgesic systems in anesthesia

Lü

Nelson

Franks

et al. 2008

J of Comparative Neurology

218

190

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Classical anesthetics of the γ-aminobutyric acid type A receptor (GABA A )-enhancing class (e.g., pentobarbital, chloral hydrate, muscimol, and ethanol) produce analgesia and unconsciousness (sedation). Dissociative anesthetics that antagonize the N-methyl-D-aspartate (NMDA) receptor (e.g., ketamine, MK-801, dextromethorphan, and phencyclidine) produce analgesia but do not induce complete loss of consciousness. To understand the mechanisms underlying loss of consciousness and analgesia induced by general anesthetics, we examined the patterns of expression of c-Fos protein in the brain and correlated these with physiological effects of systemically administering GABAergic agents and ketamine at dosages used clinically for anesthesia in rats. We found that GABAergic agents produced predominantly delta activity in the electroencephalogram (EEG) and sedation. In contrast, anesthetic doses of ketamine induced sedation, followed by active arousal behaviors, and produced a faster EEG in the theta range. Consistent with its behavioral effects, ketamine induced Fos expression in cholinergic, monoaminergic, and orexinergic arousal systems and completely suppressed Fos immunoreactivity in the sleep-promoting ventrolateral preoptic nucleus (VLPO). In contrast, GABAergic agents suppressed Fos in the same arousal-promoting systems but increased the number of Fosimmunoreactive neurons in the VLPO compared with waking control animals. All anesthetics tested induced Fos in the spinally projecting noradrenergic A5-7 groups. 6-hydroxydopamine lesions of the A5-7 groups or ibotenic acid lesions of the ventrolateral periaqueductal gray matter (vlPAG) attenuated antinociceptive responses to noxious thermal stimulation (tail-flick test) by both types of anesthetics. We hypothesize that neural substrates of sleep-wake behavior are engaged by low-dose sedative anesthetics and that the mesopontine descending noradrenergic cell groups contribute to the analgesic effects of both NMDA receptor antagonists and GABA A receptor-enhancing anesthetics. Anesthetics that modulate the γ-aminobutyric acid type A receptor (GABA A ; by direct gating of the Cl channel or by potentiating the effects GABA; hereafter referred to as GABA A agents) induce both analgesia and loss of consciousness (sedation) and are associated with a slow-wave electroencephalogram (EEG) pattern and depressed CNS function (for review see Sloan, 1998). In contrast, anesthetics that act by antagonizing Nmethyl-D-aspartate (NMDA) receptors (e.g., ketamine, MK-801, phencyclidine, dextromethorphan, and nitrous oxide) produce analgesia but also preserve some aspects of consciousness (dissociative anesthesia). These NMDA receptor antagonist anesthetics are associated, especially at subanesthetic doses, with a fast, theta-range EEG (5-7 Hz) and maintenance of sympathetic tone (Yamamura et al., 1981;Carruba et al., 1987;Marquis et al., 1989;Sagratella et al., 1992; Mattia and Moreton, 1996). There is an increase in the EEG delta power (<4 Hz) during subsequent episodes of slee...

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“…Lesions of these relay nuclei have been shown to disrupt or compromise circadian entrainment of other brain regions (e.g., DMH lesions abolish circadian changes in spontaneous LC firing patterns) (5). Furthermore, lesions of sPVZ greatly dampen or abolish circadian rhythms of body temperature, sleep, and/or locomotor activity (6).…”

Section: Discussionmentioning

confidence: 99%

Two forces for arousal: Pitting hunger versus circadian influences and identifying neurons responsible for changes in behavioral arousal

Ribeiro

Sawa

Carren-LeSauter

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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The mechanisms underlying CNS arousal in response to homeostatic pressures are not known. In this study, we pitted two forces for CNS arousal against each other (circadian influences vs. restricted food availability) and measured the neuronal activation that occurs in a behaviorally defined group of animals that exhibited increased arousal in anticipation of feeding restricted to their normal sleeping time. The number of c-FOS؉ neurons was significantly increased only in the ventromedial nucleus of the hypothalamus (VMH) in these mice, compared with control animals whose feeding was restricted to their normal active and feeding time (P < 0.01). Because the activation of VMH neurons coincides with the earliest signs of behavioral arousal preceding a change in meal time, we infer that VMH activation is involved in the increased arousal in anticipation of food.T he activation of behavior is driven by homeostatically regulated variables, such as hunger and circadian rhythms. The problem of exactly how these two types of influences interact to modulate behavior has been stated (1) but not solved. Mechanisms for changes in CNS arousal have remained controversial.We pitted two forces for CNS arousal against each other (food availability vs. circadian influences) and searched for the first neuronal activation that occurs in animals as they began to change their activation of behavior from a circadian light-driven rhythm to one dictated by restricted food availability.The present study (i) takes into account the individual differences in food anticipatory activity and links those to neuronal activation; (ii) pits the homeostatic drive for feeding against the circadian drive to rest during the light period, thus enabling a cell-by-cell dissection of these two pathways; (iii) has a control group that is exposed to the same restricted feeding paradigm as the test group, for the same number of days, with the difference that control animals receive their daily meal during their behaviorally active period; (iv) conceptualizes the problem as one of generalized CNS arousal; and (v) examines animals' brains as close to the development of the food anticipatory activity as possible. This design was intended to identify the earliest neuronal changes, and therefore the most likely to be causing these behavioral changes. ResultsShifted animals were significantly more active in the 3-h period preceding the shifted food presentation time, compared with controls. In fact, running wheel revolutions were increased from 314 Ϯ 151 in nonshifted animals to 1,768 Ϯ 398 in shifted animals (P Ͻ 0.01) (Figs. 1 and 2 and Table 1).We examined neuronal activation, as measured by c-FOS expression, in every neuronal group that could be conceived, based on the literature (see Discussion), as mediating these changes in the timing of the activation of behavior [16 regions: medial preoptic area (MPA), ventrolateral preoptic nucleus (VLPO), medial part of the medial preoptic nucleus (MPOM), lateral hypothalamus (LH), subparaventricular zone (sPVZ), paraven...

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Contrasting Effects of Ibotenate Lesions of the Paraventricular Nucleus and Subparaventricular Zone on Sleep–Wake Cycle and Temperature Regulation

Cited by 299 publications

References 38 publications

Circadian regulation of lipid metabolism

Circadian regulation of lipid metabolism

Role of endogenous sleep‐wake and analgesic systems in anesthesia

Two forces for arousal: Pitting hunger versus circadian influences and identifying neurons responsible for changes in behavioral arousal

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