Selective serotonin reuptake inhibitors and raft inhibitors shorten the period of Period1-driven circadian bioluminescence rhythms in rat-1 fibroblasts

Nomura, Kazumi; Castanon-Cervantes, Oscar; Davidson, Alec J.; Fukuhara, Chiaki

doi:10.1016/j.lfs.2008.03.024

Cited by 30 publications

(23 citation statements)

References 38 publications

(57 reference statements)

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“…Different selective serotonin reuptake inhibitors were found to significantly shorten circadian period in SCN and accelerate damping rate in fibroblasts [101]. In rodents, fluoxetine was shown to advance SCN phase [102] and to modulate both serotonin and lightinduced phase shifts [103,104].…”

Section: Antidepressant Drugsmentioning

confidence: 99%

Chronobiology of Bipolar Disorder: Therapeutic Implication

Dallaspezia

Benedetti

2015

Curr Psychiatry Rep

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Multiple lines of evidence suggest that psychopathological symptoms of bipolar disorder arise in part from a malfunction of the circadian system, linking the disease with an abnormal internal timing. Alterations in circadian rhythms and sleep are core elements in the disorders, characterizing both mania and depression and having recently been shown during euthymia. Several human genetic studies have implicated specific genes that make up the genesis of circadian rhythms in the manifestation of mood disorders with polymorphisms in molecular clock genes not only showing an association with the disorder but having also been linked to its phenotypic particularities. Many medications used to treat the disorder, such as antidepressant and mood stabilizers, affect the circadian clock. Finally, circadian rhythms and sleep researches have been the starting point of the developing of chronobiological therapies. These interventions are safe, rapid and effective and they should be considered first-line strategies for bipolar depression.

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Section: Antidepressant Drugsmentioning

confidence: 99%

Chronobiology of Bipolar Disorder: Therapeutic Implication

Dallaspezia

Benedetti

2015

Curr Psychiatry Rep

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“…Investigators have suggested that neurotransmitter signaling may occur via clustering of receptors in lipid rafts or caveolae, and the effects of lipid rafts on neurotransmitter signaling have been implicated in neurological and psychiatric diseases in general (Nomura et al , 2008, Pani and Singh, 2009), and in mood disorders in particular (Brambilla et al , 2003, Shiah and Yatham, 2000, Donati et al , 2008). Traditionally, the brain systems receiving the greatest attention in neurobiological studies of mood disorders were the monoaminergic neurotransmitter systems (e.g., the serotonergic, dopaminergic, and norepinephrinergic systems) that are extensively distributed throughout the network of limbic, striatal, hippocampal, and prefrontal cortical neuronal circuits (Drevets, 2000, Manji and Duman, 2001, Nestler et al , 2002).…”

Section: Stress and Sleep Deprivation Cause Oxidative Damage To Mitocmentioning

confidence: 99%

The Role of Nutrients in Protecting Mitochondrial Function and Neurotransmitter Signaling: Implications for the Treatment of Depression, PTSD, and Suicidal Behaviors

Zhu

Bao

et al. 2014

Critical Reviews in Food Science and Nutrition

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Numerous studies have linked severe stress to the development of major depressive disorder (MDD), and suicidal behaviors. Furthermore, recent preclinical studies from our laboratory and others have demonstrated that in rodents, chronic stress and the stress hormone cortisol has caused oxidative damage to mitochondrial function and membrane lipids in the brain. Mitochondria play a key role in synaptic neurotransmitter signaling by providing adenosine triphosphate (ATP), mediating lipid and protein synthesis, buffering intracellular calcium, and regulating apoptotic and resilience pathways. Membrane lipids are similarly essential to central nervous system (CNS) function, because cholesterol, polyunsaturated fatty acids, and sphingolipids form a lipid raft region, a special lipid region on the membrane that mediates neurotransmitter signaling through G-protein coupled receptors and ion channels. Low serum cholesterol levels, low antioxidant capacity, and abnormal early morning cortisol levels are biomarkers consistently associated with both depression and suicidal behaviors. In this review, we summarize the manner in which nutrients can protect against oxidative damage to mitochondria and lipids in the neuronal circuits associated with cognitive and affective behaviors. These nutrients include ω3 fatty acids, antioxidants (vitamin C and zinc), members of the vitamin B family (Vitamin B12 and folic acid) and magnesium. Accumulating data have shown that these nutrients can enhance neurocognitive function, and may have therapeutic benefits for depression and suicidal behaviors. A growing body of studies suggests the intriguing possibility that regular consumption of these nutrients may help prevent the onset of mood disorders and suicidal behaviors in vulnerable individuals, or significantly augment the therapeutic effect of available antidepressants. These findings have important implications for the health of both military and civilian populations.

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“…Selective serotonin reuptake inhibitors affect circadian phase (Nomura et al, 2008). Serotoninergic cell bodies appear in the suprachiasmatic nuclei of hamsters that have been held in constant darkness, while serotonergic cells are absent in the suprachiasmatic nuclei of animals that have been bilaterally enucleated (Yamazaki et al, 1999).…”

Section: Discussionmentioning

confidence: 99%