Circadian tryptophan hydroxylase levels and serotonin release in the suprachiasmatic nucleus of the rat

Barassin, Stéphane; Raison, Sylvie; Saboureau, Michel; Bienvenu, Christèle; Maître, Michel; Малан, А.; Pévet, Paul

doi:10.1046/j.1460-9568.2002.01928.x

Cited by 65 publications

(50 citation statements)

References 48 publications

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“…Indeed some of the major neurotransmitters that have been implicated in mood regulation, including serotonin, norepinephrine and dopamine, have a circadian rhythm in their levels, release, and synthesis-related enzymes (Weiner et al, 1992;Shieh et al, 1997;Aston-Jones et al, 2001;Barassin et al, 2002;Khaldy et al, 2002;Castaneda et al, 2004;Weber et al, 2004;Malek et al, 2005). There are also circadian rhythms in the expression and activity of several of the receptors that bind these neurotransmitters, suggesting that these entire circuits are under circadian control (Kafka et al, 1983;Wesemann and Weiner, 1990;Witte and Lemmer, 1991;Coon et al, 1997;Akhisaroglu et al, 2005).…”

Section: Influence Of the Molecular Clock On Mood-related Neurotransmmentioning

confidence: 99%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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For many years, researchers have suggested that abnormalities in circadian rhythms may underlie the development of mood disorders such as bipolar disorder, major depression and seasonal affective disorder. Furthermore, some of the treatments that are currently employed to treat mood disorders are thought to act by shifting or "resetting" the circadian clock, including total sleep deprivation and bright light therapy. There is also reason to suspect that many of the mood stabilizers and antidepressants used to treat these disorders may derive at least some of their therapeutic efficacy by affecting the circadian clock. Recent genetic, molecular and behavioral studies implicate individual genes that make up the clock in mood regulation. As well, important functions of these genes in brain regions and neurotransmitter systems associated with mood regulation is becoming apparent. In this review, the evidence linking circadian rhythms and mood disorders, and what is known about the underlying biology of this association, is presented.

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Section: Influence Of the Molecular Clock On Mood-related Neurotransmmentioning

confidence: 99%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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“…These results suggest that the experiment created long-term stress effects, which may be caused by the actual experiment or the disturbations in the circadian rhythm. Moreover, the serotonin concentration is shown to peak at the end of the light phase in rodent brain [60][61][62]. Therefore, we must consider the possibility that the sample collection time was not optimal for serotonin concentration levels in this study.…”

Section: Discussionmentioning

confidence: 99%

Transcranial Light Alters Melanopsin and Monoamine Production in Mouse (Mus musculus) Brain

et al. 2017

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Background: The mammalian circadian system sets a rhythm for the appropriate occurrence of physiological and behavioral phenomena during a 24-h period. Since the duration of the circadian system is usually less or more than 24 h, it must be entrained regularly and light is the governing stimulus of the rhythm. The target for light stimulus is the master circadian clock, which is located in the suprachiasmatic nucleus in the hypothalamus. One of the key molecules transmitting light information and entraining the clock is melanopsin (OPN4), a G protein-coupled molecule that is found most abundantly in the retina and brain. Although light stimulus is usually mediated through the eyes, light has an ability to penetrate the skull. Here, we present the effect of transcranial light illumination on OPN4 and serotonin expression in the mouse brain.

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“…However, in addition to sleep-dependent changes in neuromodulators, there also are documented circadian-dependent changes in neuromodulators. For example, serotonin levels in the pineal gland and the suprachiasmatic nucleus are lower in rats during the light cycle than during the dark cycle, and this difference appears to be controlled by circadian variation in adrenergic signaling (4,12,25,37,38). It is not known whether there are circadian variations in PRG cholinergic, adrenergic, and serotonin neuromodula- tion, but on the basis of our present findings, coupled with documented circadian variations in breathing (28,35), further studies are warranted on circadian variation of cholinergic modulation of PRG neurons.…”

Section: Discussionmentioning

confidence: 99%

A role for the Kölliker-Fuse nucleus in cholinergic modulation of breathing at night during wakefulness and NREM sleep

Bonis

Neumueller

Krause

et al. 2010

Journal of Applied Physiology

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To probe further the contributions of cholinergic rostral pontine systems in control of breathing, we designed this study to test the hypothesis that microdialysis (MD) of the muscarinic receptor antagonist atropine into the pontine respiratory group (PRG) would decrease breathing more in animals while awake than while in NREM sleep. In 16 goats, cannulas were bilaterally implanted into rostral pontine tegmental nuclei (n ϭ 3), the lateral (n ϭ 3) or medial (n ϭ 4) parabrachial nuclei, or the Kölliker-Fuse nucleus (KFN; n ϭ 6). After Ͼ2 wk of recovery from surgery, the goats were studied during a 45-min period of MD with mock cerebrospinal fluid (mCSF), followed by at least 30 min of recovery and a second 45-min period of MD with atropine. Unilateral and bilateral MD studies were completed during the day and at night. MD of atropine into the KFN at night decreased pulmonary ventilation and breathing frequency and increased inspiratory and expiratory time by 12-14% during both wakefulness and NREM sleep. However, during daytime studies, MD of atropine into the KFN had no effect on these variables. Unilateral and bilateral nighttime MD of atropine into the KFN increased levels of NREM sleep by 63 and 365%, respectively. MD during the day or at night into the other three pontine sites had minimal effects on any variable studied. Finally, compared with MD of mCSF, bilateral MD of atropine decreased levels of acetylcholine and choline in the effluent dialysis fluid. Our data support the concept that the KFN is a significant contributor to cholinergically modulated control of breathing and sleep.non-rapid eye movement sleep; pons FOR MANY YEARS, ACETYLCHOLINE (ACh) has been known to play a role in the control of breathing (14) and sleep (3). In the medial pontine reticular formation (mPRF), endogenous ACh release causes state-dependent changes in respiratory control (2) and can stimulate rapid eye movement (REM) sleep (22). Microadministration of the cholinergic agonists carbachol (mixed cholinergic agonist), bethanechol (muscarinic agonist), and neostigmine (acetylcholine esterase inhibitor) into the mPRF are all known to generate this effect (1,2,18,22,27), whereas the muscarinic antagonist atropine can block this effect (1). Indeed, mPRF cholinoceptive mechanisms can cause state-dependent changes in the firing rates of respiratory neurons in the parabrachial nuclei (16). These studies provide evidence of anatomic connectivity from the mPRF to the pontine respiratory group (PRG). Evidence of projections in the reverse direction, from the PRG to the mPRF, is provided by microinjection of fluorescent dyes into the PRG, resulting in ipsi-and contralateral positive regions in the mPRF as well as in the dorsal respiratory group and ventral respiratory group in the medulla (20). However, studies of the connectivity between brain stem respiratory neurons performed using chronically implanted arrays of microelectrodes emphasized "a sparse distribution of functional connections," which suggests that interactions between brai...

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Circadian tryptophan hydroxylase levels and serotonin release in the suprachiasmatic nucleus of the rat

Cited by 65 publications

References 48 publications

Circadian genes, rhythms and the biology of mood disorders

Circadian genes, rhythms and the biology of mood disorders

Transcranial Light Alters Melanopsin and Monoamine Production in Mouse (Mus musculus) Brain

A role for the Kölliker-Fuse nucleus in cholinergic modulation of breathing at night during wakefulness and NREM sleep

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