Afferents to the Ventrolateral Preoptic Nucleus

Chou, Tom; Bjørkum, Alvhild Alette; Gaus, Stephanie E.; Lü, Jun; Scammell, Thomas E.; Saper, Clifford B.

doi:10.1523/jneurosci.22-03-00977.2002

Cited by 437 publications

(319 citation statements)

References 46 publications

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“…Axons from the VLPO innervate cell bodies and dendrites of the noradrenergic locus coeruleus (LC), the serotonergic dorsal raphe nucleus (DRN), the histaminergic tuberomammillary nucleus (TMN), and also terminate within cholinergic cell groups of basal forebrain and the latero-dorsal/pedunculo-pontine tegmental (LDT/PPT) areas of the brain stem [75][76][77][78]. On the other hand, the VLPO receives afferents from each of the major monoaminergic systems [79]. These reciprocal connections suggest that VLPO activity is suppressed by the same arousal systems (see below) that it inhibits during sleep.…”

Section: Neural Systems Promoting Sleepmentioning

confidence: 99%

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Landolt

2008

CPD

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Abstract:To better understand the neurobiology of sleep disorders, detailed understanding of circadian and homeostatic sleep-wake regulation in healthy volunteers is mandatory. Sleep physiology and the repercussions of experimentallyinduced sleep deprivation on sleep and waking electroencephalogram (EEG), vigilance and subjective state are highly variable, even in healthy individuals. Accumulating evidence suggests that many aspects of normal sleep-wake regulation are at least in part genetically controlled. Current heritability estimates of sleep phenotypes vary between approximately 20-40 % for habitual sleep duration, to over 90 % for the spectral characteristics of the EEG in nonREM sleep. The molecular mechanisms underlying the trait-like, inter-individual variation are virtually unknown, and the human genetics of normal sleep is only at the beginning of being explored. The first studies identified distinct polymorphisms in genes contributing to the endogenous circadian clock and neurochemical systems previously implicated in sleep-wake regulation, to modulate sleep architecture and sleep EEG, vulnerability to sleep loss, and subjective and objective effects of caffeine on sleep. These insights are reviewed here. They disclose molecular mechanisms contributing to normal sleep-wake regulation in humans, and have potentially important implications for the neurobiology of sleep-wake disorders and their pharmacological treatment.

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Section: Neural Systems Promoting Sleepmentioning

confidence: 99%

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Landolt

2008

CPD

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“…DMH has the most extensive projections to arousalpromoting brain regions, including the dorsal raphe nucleus, TMN, LC, LH/PeF, and laterodorsal tegmental nucleus. In addition, DMH also has direct projections to the sleep-active VLPO and MnPO (3,4). A third major projection from the SCN is to sPVZ.…”

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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“…73 On the other hand, the increased discharge of locus coeruleus neurons that occurs during wakefulness 66 appears sufficient to cause awakening, and may be necessary for the normal duration of the wakefulness episodes. 74 The neurons of the locus coeruleus project to 32 and inhibit 75 neurons of the hypothalamic ventrolateral preoptic nucleus, which, as discussed above, is a key structure for NREM sleep. 31 In turn, neurons of the ventrolateral preoptic nucleus send inhibitory projections to the locus coeruleus.…”

Section: Integration Of the Neural And Cardiovascular Events Of Awakementioning

confidence: 99%

“…31 All of these structures receive synaptic projections from the group of hypothalamic neurons that release the orexin peptides. 32,33 The loss of orexin neurons underlies narcolepsy with cataplexy, 34 a severe neurological disorder presently classified as narcolepsy type 1 (NT1). 35 The cardiovascular events of awakening from NREM sleep…”

Section: Cardiovascular Control During Nrem Sleepmentioning

confidence: 99%

“…85 The orexin neurons also project to the ventrolateral preoptic nucleus. 32 However, orexin microinjections in the ventrolateral preoptic nucleus increase wakefulness, suggesting that orexin neuron projections exert a net inhibitory effect on neurons of the ventrolateral preoptic nucleus through local circuits. 86 In turn, the orexin neurons receive inhibitory projections from the hypothalamic ventrolateral preoptic nucleus 87 and excitatory projections from the parabrachial nucleus, 88 but minimal or absent input from the dorsal raphe and locus coeruleus.…”

Section: Integration Of the Neural And Cardiovascular Events Of Awakementioning

confidence: 99%

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Orexins and the cardiovascular events of awakening

Silvani

2017

Temperature

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This brief review aims to provide an updated account of the cardiovascular events of awakening, proposing a testable conceptual framework that links these events with the neural control of sleep and the autonomic nervous system, with focus on the hypothalamic orexin (hypocretin) neurons. Awakening from non-rapid-eye-movement sleep entails coordinated changes in brain and cardiovascular activity: the neural "flip-flop" switch that governs state transitions becomes biased toward the ascending arousal systems, arterial blood pressure and heart rate rise toward waking values, and distal skin temperature falls. Arterial blood pressure and skin temperature are sensed by baroreceptors and thermoreceptors and may positively feedback on the brain wake-sleep switch, thus contributing to sharpen, coordinate, and stabilize awakening. These effects may be enhanced by the hypothalamic orexin neurons, which may modulate the changes in blood pressure, heart rate, and skin temperature upon awakening, while biasing the wake-sleep switch toward wakefulness through direct neural projections. A deeper understanding of the cardiovascular events of awakening and of their links with skin temperature and the wake-sleep neural switch may lead to better treatments options for patients with narcolepsy type 1, who lack the orexin neurons.

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Afferents to the Ventrolateral Preoptic Nucleus

Cited by 437 publications

References 46 publications

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

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

Orexins and the cardiovascular events of awakening

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