Body temperature and locomotor activity as marker rhythms of aging of the circadian system in rodents

Mailloux, Adam W.; Benstaali, C.; Bogdan, André; Auzéby, A; Touitou, Yvan

doi:10.1016/s0531-5565(99)00051-0

Cited by 30 publications

(12 citation statements)

References 28 publications

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“…Various studies show that the body temperature has a comparable course of time over the day [ 129 , 130 , 131 , 132 ] with a minor decrease in amplitude in some individuals [ 128 , 130 ] (for a more detailed discussion of the circadian rhythm, see Section 4.1 ). Comparable results have been found in mice [ 133 ] and rats [ 134 ].…”

Section: Physiological Propertiessupporting

confidence: 64%

Robustness during Aging—Molecular Biological and Physiological Aspects

Barth

Sieber

Stark

et al. 2020

Cells

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Understanding the process of aging is still an important challenge to enable healthy aging and to prevent age-related diseases. Most studies in age research investigate the decline in organ functionality and gene activity with age. The focus on decline can even be considered a paradigm in that field. However, there are certain aspects that remain surprisingly stable and keep the organism robust. Here, we present and discuss various properties of robust behavior during human and animal aging, including physiological and molecular biological features, such as the hematocrit, body temperature, immunity against infectious diseases and others. We examine, in the context of robustness, the different theories of how aging occurs. We regard the role of aging in the light of evolution.

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Section: Physiological Propertiessupporting

confidence: 64%

Robustness during Aging—Molecular Biological and Physiological Aspects

Barth

Sieber

Stark

et al. 2020

Cells

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“…Old and young rats have not previously been studied simultaneously under other photoperiod conditions. Moreover, because of the age-related changes in circadian rhythm amplitude and phase that have been described in most species [14,32], it has been assumed that aging makes entrainment to a different LD cycle more difficult. To our knowledge, experimental verification of this hypothesis has been sparse.…”

Section: Discussionmentioning

confidence: 99%

“…These most often include an overall decreased amplitude, modification in the phase -advance or delay -of the rhythms (resulting in internal desynchronization), alteration in the free-running period and reduced sensitivity of the circadian pacemaker to photic and nonphotic signals [14,32,33,34].…”

Section: Introductionmentioning

confidence: 99%

Effect of a short photoperiod on circadian rhythms of body temperature and motor activity in old rats

Benstaali¹,

Bogdan²,

Touitou³

2002

Pflügers Arch - Eur J Physiol

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Circadian rhythms of body temperature and motor activity were documented in young and old rats (four 8-week-old and five 22-month-old male Wistars, implanted with telemetric probes and housed in a chronobiological facility) under two different photoperiod conditions. The animals were maintained in a light:dark (LD) cycle of 12 h each (LD 12:12) for 4 weeks and then exposed to a LD 6:18 cycle for 7 weeks to assess the effect of age on the desynchronization of the temporal structure of the rhythms. In old rats under LD 12:12, the power of the 24-h component and the circadian amplitude of body temperature and motor activity were markedly lower than in the young and both rhythms were phase-advanced. After the shift to LD 6:18, the circadian rhythmicity was maintained for both variables and the same phase delay (+5+/-1 h) was observed in both age groups, as was a gradual expansion of the patterns of both functions with the longer night. The photoperiod reduction (6 weeks under LD 6:18) did not modify the power of the 24-h component of body temperature and motor activity in old rats. In young rats, however, the power and amplitude of the 24-h component of motor activity rhythm fell to the levels of those in old rats, while the power of the 24-h component of body temperature rhythm and the amplitude did not change. Our data show that the circadian rhythm of motor activity, but not of body temperature, responds age dependently to a photoperiod reduction.

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“…[31]). Changes in the intrinsic free‐running period of the clock during aging have been reported but remain equivocal [32–34]. In addition, aged people frequently show a spontaneous internal desynchronization of rhythms [32].…”

Section: Circadian Rhythms Disruptions In Agingmentioning

confidence: 99%

The human pineal gland and melatonin in aging and Alzheimer's disease

Swaab

2004

Journal of Pineal Research

322

198

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The human pineal gland and melatonin in aging and Alzheimer's disease Pineal gland and melatoninIn humans, the pineal gland is 5 mm long, 1-4 mm thick and weighs about 100 mg, both in men and in women [1]. The pineal gland contains two major cell types: neuroglial cells and the predominant pinealocytes that produce melatonin.The pineal gland is a central structure in the circadian system that is innervated by a neural multi-synaptic pathway originating in the suprachiasmatic nucleus (SCN) that is located in the anterior hypothalamus. The SCN is the major circadian pacemaker of the mammalian brain and plays a central role in the generation and regulation of biological rhythms [2,3]. The pineal gland produces melatonin in a marked circadian fashion [4], reflecting signals originating in the SCN. The human SCN innervates only a small number of hypothalamic nuclei directly [5,6]. However, it may impose circadian fluctuations indirectly on the organism by means of melatonin released from the pineal gland [7].The biosynthetic pathway of pineal melatonin has been studied thoroughly. l-Tryptophan is taken up from the circulation and converted to serotonin (5-HT) by tryptophan hydroxylase. 5-HT is metabolized by the rate-limiting enzyme arylalkylamine N-acetyltransferase (AA-NAT) to N-acetyl-5-hydroxytryptamine, and in turn by hydroxyindole-o-methyltransferase to melatonin. 5-HT can also be oxidized by monoamine oxidase A (MAOA) to 5-hydroxyindoleacetic acid [4,8]. In all vertebrates, the activity of the rhythm-generating enzyme AA-NAT increases at night by a factor 7-150, depending on the species. The molecular mechanisms regulating AA-NAT are also remarkably different among species. For instance, in the rat, pineal AA-NAT is regulated at both mRNA level and protein level; however, in sheep and rhesus macaque, pineal AA-NAT mRNA levels show relatively little change over a 24-hr period and changes in AA-NAT activity are primarily regulated at the protein level [9,10]. In the human pineal gland, significant daily fluctuations in AA-NAT mRNA levels were not detected either [11], which suggests that pineal AA-NAT activity may be mainly regulated on the post-transcriptional level in human.The main environmental control of the pineal melatonin synthesis is light intensity. Light perceived by the retina reaches the SCN through the retinohypothalamic tract, which has been revealed by an in vitro postmortem tracing procedure, also in the human hypothalamus [12]. The SCN innervates the pineal gland via the dorsomedial hypothalamic nucleus, the upper thoracic intermediolateral cell columns of the spinal cord and the superior cervical ganglia (SCG), resulting in the rhythmic secretion of melatonin [13,14]. The importance of ocular light as a temporal cue has been clearly demonstrated in circadian studies of blind Abstract: The pineal gland is a central structure in the circadian system which produces melatonin under the control of the central clock, the suprachiasmatic nucleus (SCN). The SCN and the output of the pineal gland, i.e....

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Body temperature and locomotor activity as marker rhythms of aging of the circadian system in rodents

Cited by 30 publications

References 28 publications

Robustness during Aging—Molecular Biological and Physiological Aspects

Robustness during Aging—Molecular Biological and Physiological Aspects

Effect of a short photoperiod on circadian rhythms of body temperature and motor activity in old rats

The human pineal gland and melatonin in aging and Alzheimer's disease

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