Monoamine depletion blocks triazolam-induced phase advances of the circadian clock in hamsters

Penev, Plamen D.; Zee, Phyllis C.; Turek, Fred W.

doi:10.1016/0006-8993(94)91241-6

Cited by 30 publications

(6 citation statements)

References 48 publications

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“…It seems likely that this accounts for the loss of shifting in hamsters given triazolam 10 days after receiving the neurotoxin 5,7-DHT (Cutrera, Kalsbeek & Pevet, 1994). Similar experiments (Penev, Zee & Turek, 1994) with a non-specific monoamine depletor, reserpine, must be treated with similar caution; monoamines in the hypothalamus were not depleted more than 76 yo but locomotor activity was much reduced by the reserpine treatment. The latter may well be responsible for the loss of shifting.…”

Section: Physiological Mechanismsmentioning

confidence: 96%

Locomotor Activity and Non‐photic Influences on Circadian Clocks

1996

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Some of the main themes in this review are as follows. 1. The notion that non-photic zeitgebers are weak needs re-examining. Phase-shifts to some non-photic manipulations can be as large as those to light pulses. 2. As well as being able to phase-shift and entrain free-running rhythms, non-photic events have a number of other effects: these include after-effects of entrainment, period changes, and promotion of splitting. 3. The critical variable for non-photic shifting is unknown. Locomotor activity is more likely to be an index of some other necessary state rather than being causal itself. This index may be better when tendencies to move are channelled into easily measured behaviours like wheel-running. 4. Given ignorance about the critical variable, quantification of activity may be the best presently available measure of zeitgeber intensity. Therefore, the behaviour during non-photic manipulations must be examined as carefully as the shifts themselves. When no phase-shifting follows manipulations such as IGL lesions or serotonin depletion, if the animals are inactive, then little can be inferred. 5. Lack of information on the critical variable(s) for non-photic shifting makes it problematic to compare data from studies using different non-photic manipulations. However, the presence of locomotor activity (or its correlate) does appear to be necessary for triazolam to produce shifts. 6. Novelty-induced wheel-running in hamsters depends on the NPY projection from the IGL to SCN. It remains to be determined how important NPY is in other species or in clock-resetting by other manipulations, but methods are now available to study this. 7. Interactions between photic and non-photic zeitgebers remain virtually unexplored, but it is evident that photic and non-photic stimuli can attenuate the phase-shifting effects of each other. Interactions are not purely additive or predictable from PRCs. 8. The circadian system does more than synchronize free-running rhythms to the solar day. Its non-photic functions and their interactions with photic inputs probably account for some of the anatomical complexity of circadian circuitry.

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Section: Physiological Mechanismsmentioning

confidence: 96%

Locomotor Activity and Non‐photic Influences on Circadian Clocks

1996

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“…A small number of previous studies have examined the effects of manipulating the noradrenergic system pharmacologically on circadian rhythms. Penev et al (1993Penev et al ( , 1994 reported that monoamine depletion inhibits wheel running, phase advanced behavioural rhythms in LD, lengthened free-running period and attenuated photically and non-photically induced phase advances. Chronic treatment with the ␣-1 agonist clonidine resulted in a significant shortening of the free-running period of rats, an effect that was reversed upon washout (Rosenwasser, 1989(Rosenwasser, , 1996.…”

Section: Putative Mechanisms Of Atomoxetine Actions Of Circadian Rhythmsmentioning

confidence: 99%

The noradrenaline reuptake inhibitor atomoxetine phase-shifts the circadian clock in mice

O'Keeffe¹,

Thome²,

Coogan³

2012

Neuroscience

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Circadian rhythms are recurring cycles in physiology and behaviour that repeat with periods of near 24 h and are driven by an endogenous circadian timekeeping system with a master circadian pacemaker located in the suprachiasmatic nucleus (SCN). Atomoxetine is a specific noradrenaline reuptake inhibitor that is used in the clinical management of attention-deficit/hyperactivity disorder (ADHD). In the current study we examined the effects of atomoxetine on circadian rhythms in mice. Atomoxetine (i.p.; 3 mg/kg) treatment of mice free-running in constant light (LL) at circadian time (CT) 6 induced large phase delays that were significantly different to saline controls. Treatment of animals with atomoxetine at CT13 or CT18 did not elicit any significant phase shifts. We also examined the effects of atomoxetine treatment of animals free-running in constant darkness (DD). Atomoxetine treatment at CT6 in these animals leads to more modest, but significant, phase advances, whereas treatment at CT18 did not elicit significant phase shifts. The effects of atomoxetine in LL were attenuated by pretreatment with the α-1 adrenoreceptor antagonist prazosin and were mimicked by another noradrenaline reuptake inhibitor, reboxetine. Further, atomoxetine treatment at CT6 induced a downregulation of c-Fos and CLOCK in the SCN, but did not alter the expression of PER2 and BMAL1. Atomoxetine during the night phase did not alter any of these factors. Atomoxetine treatment preceding a light pulse at CT15 enhanced the magnitude of the photic-phase shift, whereas it altered photic induction of the immediate early gene products c-Fos and ARC in the SCN. These data indicate that atomoxetine can reset the circadian clock and indicate that part of the therapeutic profile of atomoxetine may be through circadian rhythm modulation.

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“…These changes include decreases in the amplitude of many overt rhythms, including the rhythms of locomotor activity, drinking, body temperature, and the sleep-wake cycle [19,24,28,29,34], as well as corresponding decreases in the amplitudes of at least two rhythms of suprachiasmatic nucleus (SCN, site of the master mammalian circadian pacemaker) physiology: the rhythms of neural firing rate and of glucose uptake [25,31,35]. Additionally, species-specific changes in the free-running period in constant darkness (τ) are often observed [15,21,27,28] Aging does not alter the size of the SCN or the number of neurons it contains [14,36], suggesting that the effects of age are due to changes in the pacemaking capabilities of the neurons or the connections between them.…”

Section: Introductionmentioning

confidence: 99%

Effects of age on circadian rhythms are similar in wild-type and heterozygous Clock mutant mice

Kolker

Vitaterna

Fruechte

et al. 2004

Neurobiology of Aging

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The amplitudes of many circadian rhythms, at the behavioral, physiological, cellular, and biochemical levels, decrease with advanced age. Previous studies suggest that the amplitude of the central circadian pacemaker is decreased in old animals. Recently, it has been reported that expression of several circadian clock genes, including Clock, is lower in the master circadian pacemaker of old rodents. To test the hypothesis that decreased activity of a circadian clock gene renders animals more susceptible to the effects of aging, we analyzed the circadian rhythm of locomotor activity in young and old wild-type and heterozygous Clock mutant mice. We found that the effects of age and the Clock mutation were additive. These results indicate that age-related changes in circadian rhythmicity occur equally in wild-type and heterozygous Clock mutants, suggesting that the Clock mutation does not render mice more susceptible to the effects of age on the circadian pacemaker.

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Monoamine depletion blocks triazolam-induced phase advances of the circadian clock in hamsters

Cited by 30 publications

References 48 publications

Locomotor Activity and Non‐photic Influences on Circadian Clocks

Locomotor Activity and Non‐photic Influences on Circadian Clocks

The noradrenaline reuptake inhibitor atomoxetine phase-shifts the circadian clock in mice

Effects of age on circadian rhythms are similar in wild-type and heterozygous Clock mutant mice

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