Circadian variations in expression of the trkB receptor in adult rat hippocampus

Dolci, Claudia; Montaruli, A.; Roveda, Eliana; Barajon, Isabella; Vizzotto, Laura; Zucconi, Gigliola Grassi; Carandente, F.

doi:10.1016/j.brainres.2003.09.018

Cited by 51 publications

(35 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, the expression of BDNF mRNA and protein has been found to oscillate in a circadian fashion within suprachiasmatic nucleus (SCN) of the anterior hypothalamus (28). Moreover, the expression of BDNF and TrkB display statistically significant circadian variation in rat hippocampus (29). Conceivably, BDNF/TrkB system and NAS coordinately orchestrate a variety of neuronal activities in hippocampus with a style of circadian oscillation, e.g., hippocampal neurogenesis and antidepressant.…”

Section: Discussionmentioning

confidence: 99%

N -acetylserotonin promotes hippocampal neuroprogenitor cell proliferation in sleep-deprived mice

Sompol¹,

Liu²,

Baba

et al. 2011

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

View full text Add to dashboard Cite

N-acetylserotonin (NAS), the immediate precursor of melatonin, the pineal gland indole, is regulated in a circadian rhythm. NAS swiftly activates TrkB in a circadian manner and exhibits antidepressant effect in a TrkB-dependent manner. Here we show that NAS regulates an early event of neurogenesis by increasing neuronal progenitor cell (NPC) proliferation. Subchronic and chronic NAS administration induces NPC proliferation in adult mice. Chronic NAS treatment triggers TrkB receptor activation and its downstream signaling in NPCs. Blockade of TrkB abolishes NAS-elicited neurogenesis in TrkBF616A knockin mice, suggesting that TrkB activation is essential for the effect of NAS-induced NPC proliferation. Moreover, NAS induces NPC proliferation in both active and sleeping phases of the mice. Strikingly, NAS significantly enhances NPC proliferation in sleep-deprived mice. Thus, our finding demonstrates a unique function of NAS in promoting robust NPC proliferation, which may contribute to hippocampal plasticity during sleeping period.sleep deprivation | brain-derived neurotrophic factor S erotonin N-acetyltransferase (arylalkylamine nacetyltransferase, AANAT) is an enzyme that catalyzes the metabolism of the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) into N-acetylserotonin (NAS). AANAT mRNA is predominantly expressed in the pineal gland and retina. In the pineal gland, NAS is an intermediate in the synthesis of melatonin from serotonin. Accumulating evidence suggests that NAS acts as a mediator of the antidepressant action of drugs, and chronic but not acute treatment of rats with the antidepressant fluoxetine increases the content of AANAT mRNA in the rat hippocampus (1). Consistent with this observation, it has been reported that C3H mice that possess wild-type (WT) AANAT display shorter duration of immobility than C57 BL6 mice that have a mutation in the AANAT gene and are considered as AANAT-deficient and consequently NAS-and melatonin-deficient animals (2, 3). Moreover, tail suspension tests show that administration (i.p.) of NAS reveals antidepressant effect (4, 5). Recently, we showed that NAS directly activates TrkB in a circadian manner and exhibits antidepressant effect in a TrkB-dependent way. NAS rapidly activates TrkB, but not TrkA or TrkC, in a neurotrophinand MT3 receptor-independent manner. Administration of NAS activates TrkB in brain-derived neurotrophic factor (BDNF) knockout mice. Hence, our findings support the hypothesis that NAS is more than a melatonin precursor, and that it can potently activate TrkB receptor (6).

show abstract

Section: Discussionmentioning

confidence: 99%

N -acetylserotonin promotes hippocampal neuroprogenitor cell proliferation in sleep-deprived mice

Sompol¹,

Liu²,

Baba

et al. 2011

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

View full text Add to dashboard Cite

show abstract

“…1992). The neurotrophin BDNF and its high affinity receptor TrkB also show daily changes, with higher levels during the active night period (Berchtold et al 1999;Dolci et al 2003;Pollock et al 2001;Schaaf et al 2000;Sei et al 2003). These fluctuations in molecular systems may underlie functional changes in the hippocampus that follow the day-night cycle.…”

Section: Modulation Of Cognition By Circadian Rhythmsmentioning

confidence: 99%

Age-related disruptions of circadian rhythm and memory in the senescence-accelerated mouse (SAMP8)

Pang

Miller

Fortress

et al. 2006

AGE

View full text Add to dashboard Cite

Common complaints of the elderly involve impaired cognitive abilities, such as loss of memory and inability to attend. Although much research has been devoted to these cognitive impairments, other factors such as disrupted sleep patterns and increased daytime drowsiness may contribute indirectly to impaired cognitive abilities. Disrupted sleep-wake cycles may be the result of age-related changes to the internal (circadian) clock. In this article, we review recent research on aging and circadian rhythms with a focus on the senescence-accelerated mouse (SAM) as a model of aging. We explore some of the neurobiological mechanisms that appear to be responsible for our aging clock, and consider implications of this work for age-related changes in cognition.Key words aging . C-Fos . circadian rhythms . mouse . running wheel . SAMP8 . suprachiasmatic nucleus Cognitive impairments are well-known complaints of the elderly. Despite their obvious clinical importance, many questions remain unanswered. One important issue concerns whether cognitive impairments are due to direct alterations in the cognitive function, or to other difficulties that may in turn result in cognitive deficits. For example, the elderly often report poor night-time sleep quality, daytime sleepiness, lack of energy, and difficulty adjusting to a time shift (increased "jet lag"). Could these effects contribute to cognitive impairments?Although a confluence of factors may lead to poor sleep quality, etc., it is likely that one general culprit is aging of the internal (circadian) clock that regulates these behaviors (Munch et al. 2005;Turek et al. 1995;Weitzman et al. 1982). Moreover, evidence suggests that our internal clock may also mediate cognitive functioning (Antoniadis et al. 2000;Brock 1991, Stone 1989van Gool 1986;van Someren et al. 1993a). In this article, we review recent research on aging and circadian rhythms, with a focus on the senescence-accelerated mouse line. We explore some of the neurobiological mechanisms that appear to be responsible for our aging clock, and consider implications of this work for the study of age-related changes in cognition.Circadian rhythms are predictable and regularly occurring daily changes in behavior and physiological states. The term circadian, literally meaning "around a day," has its origins in two Latin words: Circa (around) and dies (day). Two defining characteristics AGE (2006) of circadian rhythms are their continued persistence in the absence of external cues in the environment and their ability to be entrained (synchronized) by environmental cues. With respect to the former property, it is the endogenous (self-sustaining) nature of circadian rhythms that engenders an internal clock. With respect to the latter property, the major external cue that serves to synchronize the circadian rhythms of humans and other mammals is light, but almost any periodic event can act as a Zeitgeber ("time-giver").Research on the biological basis of circadian rhythms in humans and other mammals implicates the s...

show abstract

“…In recent years, many experimental studies in rats and mice indicate an endogenous cyclical change in central BDNF and trkB expressions within 24 h (Bova et al 1998, Schaaf et al 2000a, Dolci et al 2003, although the implication of these circadian oscillations still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Plasma brain-derived neurotrophic factor daily variations in men: correlation with cortisol circadian rhythm

Begliuomini

Lenzi²,

Ninni³

et al. 2008

Journal of Endocrinology

136

View full text Add to dashboard Cite

Expression and secretion of neurotrophins, including brainderived neurotrophic factor (BDNF), are regulated also by neuronal activity. Data available in the literature suggest that BDNF central levels are influenced by light and dark. Diurnal changes of BDNF mRNA and protein contents have been demonstrated in the rat central nervous system. Based on these pieces of evidence, we investigated the hypothesis of a possible diurnal variation of BDNF circulating levels in human males. Moreover, we looked for a possible correlation with cortisol circadian rhythm, since both BDNF and cortisol are implicated in the maintenance of cerebral functions. In this study, 34 healthy young male volunteers were included. Five blood samples were drawn from each subject thrice in a month at regular 4-h intervals (0800, 1200, 1600, 2000, and 2400 h). BDNF and cortisol were measured in all samples. BDNF was determined by ELISA method. Our results show that plasma BDNF levels, as well as cortisol levels, are significantly higher in the morning when compared with the night (P!0 . 001), with a trend of constant decrease during the day. Furthermore, plasma BDNF and cortisol are positively correlated (Spearman indexZ0 . 8466). The present study is the first to demonstrate the presence of a diurnal rhythm of BDNF in humans. Moreover, the correlation found out between BDNF and cortisol circadian trend allows us to speculate that these two factors may be physiologically co-regulated, in order to maintain the homeostasis of integrated cerebral activities.

show abstract

Circadian variations in expression of the trkB receptor in adult rat hippocampus

Cited by 51 publications

References 19 publications

N -acetylserotonin promotes hippocampal neuroprogenitor cell proliferation in sleep-deprived mice

N -acetylserotonin promotes hippocampal neuroprogenitor cell proliferation in sleep-deprived mice

Age-related disruptions of circadian rhythm and memory in the senescence-accelerated mouse (SAMP8)

Plasma brain-derived neurotrophic factor daily variations in men: correlation with cortisol circadian rhythm

Contact Info

Product

Resources

About