Chapter

Input pathways to the biological clock

Jens Hannibal

in Seasonal Affective Disorder

Second edition

Published on behalf of Oxford University Press

Published in print October 2009 | ISBN: 9780199544288
Published online February 2013 | e-ISBN: 9780191754593 | DOI: http://dx.doi.org/10.1093/med/9780199544288.003.0002
Input pathways to the biological clock

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Seasonal affective disorder (SAD) is a subtype of mood disorder characterized by recurrent episodes of major depression occurring with a seasonal pattern starting during the fall and winter and with full remission during the spring and summer (Rosenthal et al. 1985). It was proposed that one major reason for the development of this condition is the lack of bright light during the winter months, an early observation which developed into a treatment paradigm, and which has been used successfully for treating SAD for more than 20 years (Terman and Terman 2005). The effectiveness of light therapy has been compared and found almost equal to pharmacological treatment using antidepressant medication (Lam et al. 2006). Although bright light treatment seems to reduce depressive symptoms in SAD patients, little is known about the mechanism of light therapy. It has been hypothesized that the circadian hormone melatonin is involved in SAD. Melatonin is a “night” signal released from the pineal gland, which activates M1 and M2 receptors found in the brain clock, the suprachiasmatic nucleus (SCN), and which modulates the circadian rhythm generated by the clock (McClung 2007). Melatonin also plays an important role in seasonal physiology in many mammalian species and is strongly regulated by the SCN and by light. Measurements of dim light melatonin onset (DLMO) have been proven to be a valid marker for the circadian phase which, when compared to normal controls, is delayed in SAD patients (Lewy et al. 1998; Pandi-Perumal et al. 2007). This has led to the central hypothesis of SAD called the circadian phase shift hypothesis. This hypothesis is primarily based on research demonstrating that early morning bright light treatment of SAD is most effective, possibly due to the early morning phase advance of the clock, which in turn leads to the synchronization of the circadian rhythm, the sleep–wake cycle, and the melatonin rhythm (Lewy et al. 1987; Pandi-Perumal et al. 2007). The above-mentioned hypothesis of the circadian phase shift and the role of melatonin in SAD are still being debated.

Recent studies within the field of chronobiology have identified a new light detection system in the mammalian retina which measures environmental light intensities (irradiance) used for several so-called non-image forming (NIF) processes such as entrainment of the circadian clock and regulation of melatonin secretion from the pineal gland, masking behavior and regulation of the papillary light reflex (Fu et al. 2005). It is likely that a more detailed understanding of NIF will also increase our understanding of the role of light for patients suffering from SAD. The present chapter summarizes recent findings on the NIF neuronal pathway to the brain and two other neuronal input pathways that are able to modulate light input to the clock. The molecular clock and the structural nature of the SCN are presented in Chapter 1.

Chapter.  8030 words.  Illustrated.

Subjects: Psychiatry

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