Melatonin Signaling as a Link between Sleep and Circadian Biology: Practical Implications
Bibliographic record
Abstract
Daniel P. Cardinali UCA-BIOMED-CONICET, Faculty of Medical Sciences, Pontificia Universidad Católica Argentina, 1107 Buenos Aires, ArgentinaGregory M. Brown Centre for Addiction and Mental Health, University of Toronto, 100 Stokes St., Toronto, ON M6J 1H4, CanadaCorresponding author: Dr. Daniel P. Cardinali, UCA-BIOMED-CONICET, Faculty of Medical Sciences, Pontificia Universidad Católica Argentina, 1107 Buenos Aires, Argentina. E-mail: danielcardinali@uca.edu.ar, danielcardinali@fibertel.com.ar. Phone: +54911-44743547ABSTRACTNormal circadian rhythms are synchronized to a regular 24 h environmental light-dark cycle. Both the suprachiasmatic nucleus (SCN) and melatonin are essential for this adaptation. Melatonin exerts its chronophysiological action in part by acting through specific membrane receptors (MT1, MT2), which have been identified in SCN cells as well as in several neural and non-neural tissues. Both receptors havebeen cloned and share general features with other G protein linked receptors. Melatonin also exerts direct effects on intracellular proteins, such as calmodulin or tubulin, has strong free radical scavenger properties, which are non-receptor mediated, is an effective mitochondrial protector and may interact with proteasome to affect intracellular physiology. Within the SCN, melatonin reduces neuronal activity in a time-dependent manner. The disruption of these circadian mechanisms causes a number of sleep disorders known as circadian rhythm sleep disorders (CRSDs). CRSDs include delayed or advanced sleep phase syndromes; non-24 h sleep-wake rhythm disorder, time zone change syndrome (“jet lag”) and shift work sleep disorder. Disturbances in the circadian phase position of plasma melatonin levels have been found in all these disorders. In addition, comorbidity of severe circadian alterations with neurodegenerative diseases like Alzheimer’s disease (AD) has been documented. Currently there is sufficient evidence to implicate endogenous melatonin as an im-portant mediator in CRSD pathophysiology. The documented efficacy of melatonin to reduce chronic benzodiazepine/Z drug use in insomnia patients is also discussed.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.002 | 0.003 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; both teacher heads agree on what is shown here.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".