BDNF and trkB mRNAs oscillate in rat brain during the light–dark cycle

Bova, Rodolfo; Micheli, Maria Rita; Qualadrucci, Paolo; Zucconi, Gigliola Grassi

doi:10.1016/s0169-328x(98)00092-8

Cited by 102 publications

(59 citation statements)

References 26 publications

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“…Light:darkness cycles could in some way influence BDNF expression by modulating the cerebral circadian pacemaker localized in the SCN of the hypothalamus. It has been shown that both BDNF mRNA and protein, as well as trkB receptor, present rhythmic variations in rat CNS (Bova et al 1998, Berchtold et al 1999. Bova et al (1998) and Berchtold et al (1999) analyzed the expression of BDNF mRNA in the rat hippocampus and frontal cortex and they both observed that the highest BDNF mRNA levels were reached during the dark hours (activity period), while the lowest BDNF levels were detected during the light hours (rest period).…”

Section: Discussionmentioning

confidence: 99%

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

Begliuomini

Lenzi²,

Ninni³

et al. 2008

Journal of Endocrinology

145

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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.

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Section: Discussionmentioning

confidence: 99%

“…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

145

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“…www.learnmem.org Cirelli and Tononi 2000;Berchtold et al 2001), dietary restriction (Lee et al 2000), sleep and circadian rhythm (Bova et al 1998;Liang et al 1998;Berchtold et al 1999;Cirelli and Tononi 2000), also appear to affect BDNF gene expression. Moreover, BDNF mRNA levels could be influenced under a variety of pathological conditions known to alter neuronal activity in the brain, including Alzheimer's (Phillips et al 1991;Narisawa-Saito et al 1996;Connor et al 1997;Holsinger et al 2000), ischemia (Lindvall et al 1992;Kokaia et al 1998;Miyake et al 2002), depression (Kokaia et al 1993;Kawahara et al 1997), and stress (Smith et al 1995;Smith and Cizza 1996;Ueyama et al 1997).…”

Section: Activity-dependent Bdnf Transcription and Local Translationmentioning

confidence: 99%

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

Lu¹

2003

Learn. Mem.

849

589

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It is widely accepted that neuronal activity plays a pivotal role in synaptic plasticity. Neurotrophins have emerged recently as potent factors for synaptic modulation. The relationship between the activity and neurotrophic regulation of synapse development and plasticity, however, remains unclear. A prevailing hypothesis is that activity-dependent synaptic modulation is mediated by neurotrophins. An important but unresolved issue is how diffusible molecules such as neurotrophins achieve local and synapse-specific modulation. In this review, I discuss several potential mechanisms with which neuronal activity could control the synapse-specificity of neurotrophin regulation, with particular emphasis on BDNF. Data accumulated in recent years suggest that neuronal activity regulates the transcription of BDNF gene, the transport of BDNF mRNA and protein into dendrites, and the secretion of BDNF protein. There is also evidence for activity-dependent regulation of the trafficking of the BDNF receptor, TrkB, including its cell surface expression and ligand-induced endocytosis. Further study of these mechanisms will help us better understand how neurotrophins could mediate activity-dependent plasticity in a local and synapse-specific manner.Much of the brain's ability to adapt or modify itself in response to experience and environment lies in the plasticity of synaptic connections, both short-and long-terms. Substantial evidence indicates that the number and the strength of synapses can be changed by neuronal activity (Bliss and Collingridge 1993;Linden 1994;Malenka and Nicoll 1999;McEwen 1999). It is now widely accepted that activity-dependent modulation of synapses is critical for brain development as well as many cognitive functions in the adult. Molecular mechanisms that translate patterns of neuronal activity into specific changes in the structures and function of synapses, however, remain largely unknown. A hypothesis was put forward several years ago that neurotrophins may serve as molecular mediators for synaptic plasticity based on two observations: (1) The expression of neurotrophins is regulated by neuroelectric activity; and (2) neurotrophins could modulate the efficacy of synaptic transmission or the growth of dendrites and axons, the structural elements necessary for synaptogenesis

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“…It was shown recently that BDNF mRNA levels are higher during the dark period relative to the light period (Bova et al, 1998;Berchtold et al, 1999). However, it was unclear whether the fluctuations in BNDF expression were caused by circadian or other factors.…”

Section: The Expression Of Bdnf In the Cerebral Cortex Is High Duringmentioning

confidence: 99%

Differential Expression of Plasticity-Related Genes in Waking and Sleep and Their Regulation by the Noradrenergic System

2000

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Behavioral studies indicate that the ability to acquire long-term memories is severely impaired during sleep. It is unclear, however, why the highly synchronous discharge of neurons during sleep should not be followed by the induction of enduring plastic changes. Here we show that the expression of phosphorylated CRE-binding protein, Arc, and BDNF, three genes whose induction is often associated with synaptic plasticity, is high during waking and low during sleep. We also show that the induction of these genes during waking depends on the activity of the noradrenergic system, which is high in waking and low in sleep. These molecular results complement behavioral evidence and provide a mechanism for the impairment of long-term memory acquisition during sleep.Key words: Arc; BDNF; neural plasticity; memory; norepinephrine; P-CREB; sleep; sleep deprivation; waking Behavioral studies have shown that sleep severely impairs the ability to acquire long-term memories . For example, a large number of studies have failed to demonstrate the transfer of any learning from sleep to consecutive waking (Simon and Emmons, 1956). The retention of new information is possible only when the subject is awake during the presentation of the stimulus or when this presentation induces activation in the electroencephalogram (EEG) (Portnoff et al., 1966;Koukkou and Lehmann, 1968). Animal studies have shown that the impairment in the acquisition of long-term memories during sleep is not merely caused by a reduction of brain activity or by the reduced response to sensory inputs. In non-rapid eye movement (non-REM) sleep, neurons in the cortex and thalamus fire in synchronous bursts at overall rates only slightly lower than those in waking (Steriade, 1999). Furthermore, even if the reduced response to external stimuli is bypassed by high-frequency stimulation, hippocampal long-term potentiation (LTP) can be produced during waking but not during non-REM sleep (Leonard et al., 1987;Bramham and Srebro, 1989).From an evolutionary perspective, the suppression of long-term memory acquisition during sleep would seem to serve an adaptive purpose. In general, plastic changes leading to the acquisition of new information should occur when neural activity is related to the environment, but not when the brain is active off-line . However, the molecular correlates of the impairment of long-term memory acquisition during sleep are unclear. For example, despite the behavioral evidence against sleep learning, it has been suggested that synchronous activity bursts during non-REM sleep may be associated with massive influx of calcium and may constitute an ideal trigger for the induction of plasticityrelated genes (Buzsáki, 1998). Thus, it is of interest to establish whether genes thought to be associated with the occurrence of plastic changes are preferentially induced during waking or during sleep and, if so, what the underlying neural mechanisms might be.In this study, we examined the brain expression in sleep and waking of three molecular markers whose i...

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BDNF and trkB mRNAs oscillate in rat brain during the light–dark cycle

Cited by 102 publications

References 26 publications

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

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

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

Differential Expression of Plasticity-Related Genes in Waking and Sleep and Their Regulation by the Noradrenergic System

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