Brain‐derived neurotrophic factor and neurotrophin receptors modulate glutamate‐induced phase shifts of the suprachiasmatic nucleus

Michel, Stephan; Clark, John Patrick; Ding, Jian; Colwell, Christopher S.

doi:10.1111/j.1460-9568.2006.04972.x

Cited by 42 publications

(49 citation statements)

References 41 publications

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“…4). Since BDNF enhancement of glutamate signaling in the SCN involves TrkB receptor activation (Liang et al, 1998a;Liang et al, 2000;Michel et al, 2006;Kim et al, 2006), these data support the conclusion that ethanol blocks glutamate-induced phase delays by inhibiting BDNF-TrkB signaling. …”

supporting

confidence: 73%

“…BDNF is produced in the SCN (Liang et al, 1998b), and its signaling through TrkB receptors enhances glutamate signaling in the SCN (Michel et al, 2006). Thus, in these next experiments we investigated whether exogenous BDNF (100ng/ml) prevents ethanol inhibition of glutamate-induced phase delays.…”

Section: Bdnf Prevents Ethanol Inhibition Of Glutamate-induced Phase mentioning

confidence: 99%

“…This enhancement may involve activation of src-like kinases, which phosphorylate residues on NMDA receptor subunits (Xu et al, 2006). BDNF production in the SCN exhibits a circadian rhythm with high levels at night, and is required for nocturnal light-and glutamate-induced phase shifts (Liang et al, 2000;Allen et al, 2005;Prosser et al, 2004;Michel et al, 2006). The importance of BDNF for glutamate signaling in the SCN is further supported by results showing that addition of exogenous BDNF allows light (Liang et al, 2000) and glutamate (present results) to induce phase advances in the subjective day.…”

Section: Ethanol Affects Bdnf Signaling In the Scnmentioning

confidence: 99%

“…Another line of research suggests that increases in BDNF transcription in the hippocampus are associated with increased ethanol consumption, and that inhibiting this increase in BDNF leads to decreased ethanol consumption (McGough et al, 2004). BDNF signaling via TrkB receptors enhances NMDA receptor-generated ion currents in brain regions including the hippocampus (Levine et al, 1998;Kovalchuk et al, 2002;Kolb et al, 2005) and the SCN (Kim et al, 2006;Michel et al, 2006). This enhancement may involve activation of src-like kinases, which phosphorylate residues on NMDA receptor subunits (Xu et al, 2006).…”

mentioning

confidence: 99%

“…Given the strong inhibitory effect of acute ethanol on glutamatergic signaling (Ron, 2004;Chandler, 2003;Woodward, 2000;Krystal et al, 2003) including in the SCN (Ruby et al, 2006; data presented here), we hypothesize that ethanol enhances serotonergic phase shifts through inhibiting glutamate signaling. To test this, we co-applied DPAT with a variety of agents that inhibit photic/glutamate signaling in the SCN, including AP5, NBQX, K252a and L-NAME Ding et al, 1994;Mintz et al, 1999;Schurov et al, 1999;Michel et al, 2006;Kallingal and Mintz, 2006). In each case, the antagonist treatment enhanced DPATinduced phase advances by about 50%.…”

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confidence: 99%

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Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

2008

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Alcohol abuse is associated with sleep problems, which are often linked to circadian rhythm disturbances. However, there is no information on the direct effects of ethanol on the mammalian circadian clock. Acute ethanol inhibits glutamate signaling, which is the primary mechanism through which light resets the mammalian clock in the suprachiasmatic nucleus (SCN). Glutamate and light also inhibit circadian clock resetting induced by non-photic signals, including serotonin. Thus, we investigated the effects of acute ethanol on both glutamatergic and serotoninergic resetting of the SCN clock in vitro. We show that ethanol dose-dependently inhibits glutamate-induced phase shifts and enhances serotonergic phase shifts. The inhibition of glutamate-induced phase shifts is not affected by excess glutamate, glycine or D-serine, but is prevented by excess brain-derived neurotrophic factor (BDNF). BDNF is known to augment glutamate signaling in the SCN and to be necessary for glutamate/light-induced phase shifts. Thus, ethanol may inhibit glutamate-induced clock resetting at least in part by blocking BDNF enhancement of glutamate signaling. Ethanol enhancement of serotonergic phase shifts is mimicked by treatments that suppress glutamate signaling in the SCN, including antagonists of glutamate receptors, BDNF signaling and nitric oxide synthase. The combined effect of ethanol with these treatments is not additive, suggesting they act through a common pathway. Our data indicate further that the interaction between serotonin and glutamate in the SCN may occur downstream from nitric oxide synthase activation. Thus, acute ethanol disrupts normal circadian clock phase regulation, which could contribute to the physiological and psychological problems associated with alcohol abuse. Keywords suprachiasmatic nucleus; circadian rhythms; ethanol; glutamate; serotonin; brain-derived neurotrophic factorThe development of alcoholism and the likelihood of relapse drinking are associated with poor sleep quality and the deleterious effects of ethanol on sleep (Landolt and Gillin, 2001;Brower et al., 2001). Alcohol consumption reduces sleep quality (Kubota et al., 2002;Ehler and Slawecki, 2000;Landolt et al., 1996), which is closely linked to the circadian system. For example, the inability to fall asleep at the desired time can result from improper synchronization *Corresponding author: Dept. Biochemistry and Cellular and Molecular Biology, University of Tennessee, Knoxville, TN 37996, phone: (865) 974-2722, FAX: (865)-974-6306, rprosser@utk.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal per...

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supporting

confidence: 73%

Section: Bdnf Prevents Ethanol Inhibition Of Glutamate-induced Phase mentioning

confidence: 99%

Section: Ethanol Affects Bdnf Signaling In the Scnmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

2008

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Circadian Rhythms in Mood Disorders

McClung

2015

Circadian Medicine

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Brain‐derived neurotrophic factor/TrkB signaling regulates daily astroglial plasticity in the suprachiasmatic nucleus: Electron‐microscopic evidence in mouse

Girardet

Lebrun

Cabirol-Pol

et al. 2013

Glia

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Synchronization of circadian rhythms to the 24-h light/dark (L/D) cycle is associated with daily rearrangements of the neuronal-glial network of the suprachiasmatic nucleus of the hypothalamus (SCN), the central master clock orchestrating biological functions in mammals. These anatomical plastic events involve neurons synthesizing vasoactive intestinal peptide (VIP), known as major integrators of photic signals in the retinorecipient region of the SCN. Using an analog-sensitive kinase allele murine model (TrkB(F616A) ), we presently show that the pharmacological blockade of the tropomyosin-related kinase receptor type B (TrkB), the high-affinity receptor of brain-derived neurotrophic factor (BDNF), abolished day/night changes in the dendrite enwrapping of VIP neurons by astrocytic processes (glial coverage), used as an index of SCN plasticity on electron-microscopic sections. Therefore, the BDNF/TrkB signaling pathway exerts a permissive role on the ultrastructural rearrangements that occur in SCN under L/D alternance, an action that could be a critical determinant of the well-established role played by BDNF in the photic regulation of the SCN. In contrast, the extent of glial coverage of non-VIP neighboring dendrites was not different at daytime and nighttime in TrkB(F616A) mice submitted to TrkB inactivation or not receiving any pharmacological treatment. These data not only show that BDNF regulates SCN structural plasticity across the 24-h cycle but also reinforce the view that the daily changes in SCN architecture subserve the light synchronization process.

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Brain‐derived neurotrophic factor and neurotrophin receptors modulate glutamate‐induced phase shifts of the suprachiasmatic nucleus

Cited by 42 publications

References 41 publications

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

Acute ethanol modulates glutamatergic and serotonergic phase shifts of the mouse circadian clock in vitro

Circadian Rhythms in Mood Disorders

Brain‐derived neurotrophic factor/TrkB signaling regulates daily astroglial plasticity in the suprachiasmatic nucleus: Electron‐microscopic evidence in mouse

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