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Three different annual cycles in House Sparrows are described: temperate resident, subtropical resident, and temerpate migratory annual cycles. Photoperiodic control of the annual cycle is described, with the role of photoperiod in stimulating gonadal development discussed, along with photorefractoriness. The role of the circadian rhythm in mediating photoperiodic information is also discussed, along with the interaction of melatonin secretion by the pineal gland and the suprachiasmatic nuclei (SCN) of the hypothalamus in regulating this endogenous rhythm.

This chapter considers the challenge of accounting for the mechanisms behind seasonal photoperiodic timing in mammals for two well-defined seasonal responses: reproductive activation and the molting cycle. Topics discussed include neuroanatomical basis to the seasonal control of breeding and the molt; organization of the mammalian “photoperiodic axis”; the control of melatonin synthesis; and the link between melatonin signal transduction and deiodinase-expressing cells.

A basic understanding of how endocrine dysfunction affects the central nervous system is important for a majority of cases referred for assessment by clinical neuropsychologists. Beyond playing a role in assessment and management in more obvious scenarios, such as pituitary adenoma and Graves' disease, increasing attention is being paid to the role of neuropsychology in assessment and management of cognitive dysfunction due to illnesses with direct or indirect effects on the endocrine system and, secondarily, the central nervous system. This chapter discusses principal syndromes of the neuroendocrine system, disorders involving the thyroid hormones, diabetes mellitus, disorders involving the reproductive hormones, disorders involving the adrenal hormones, and melatonin.

Given the expanding number of associations emerging between sleep behaviour and health, measurement of sleep will become increasingly important, if not obligatory, in population-based public health research. This chapter provides the epidemiologist with a basic understanding of the physiological principles underlying sleep-wake regulation and how they might be considered when measuring sleep in epidemiological studies. Sleep is an active, rhythmic process with periodicities on multiple time scales, including homeostatic, ultradian, and circadian cycles. Measurement of sleep first of all requires a definition of what sleep is and estimates of sleep behaviour can be captured using a range of different methods. The chapter highlights possible confounding factors that might be considered when interpreting sleep data, and discusses the potential for sleep to affect the accurate measurement of other biomarkers in health research.

Like all living things, plants or animals, humans are governed by time, specifically by idiosyncratic biological clocks. They measure both daily and yearly activities in essentially all living things. These clocks regulate sleep, eating, mating, and many other life-associated behaviors. But where are biological clocks to be found? How do they work? Clocks are at the heart of modern-day phenomena such as jet lag. How did the evolutionary history of clocks cause this? We now know that clocks are centered in the brain, and they are constantly being set and adjusted in response to external light. But even single-cell organisms without eyes or brains can measure time. An analysis of organisms as diverse as mold, fruit flies, mice, and humans has allowed us to dissect biological clocks in great detail, and to define the genes responsible for this important regulator of human behavior.

Monoamine oxidase (MAO) inhibitors were introduced as antidepressants about thirty years ago. The pharmacological mechanism of their antidepressant effect was related to the inhibition of MAO activity and limitation of the catabolism of the monoamines, serotonin (5-hydroxytryptamine, 5-HT) and noradrenaline. Both monoamines play an important role in the regulation of melatonin biosynthesis from serotonin. This process involves the N-acetylation of serotonin to form N-acetylserotonin (NAS), which is catalysed by N-acetyltransferase (NAT). The synthesis of NAS is triggered by noradrenaline stimulation of the pinealocyte adrenoceptors (mainly β  ₁ receptors). The next step is methylation of NAS to form melatonin, which is catalysed by hydroxyindole-O-methyltransferase. The inhibition of MAO by MAO inhibitors is acute: it occurs within hours of the administration of a single dose. Both tricyclic and heterocyclic antidepressants increase the levels of melatonin in human plasma after administration of a single dose. A single electroconvulsive shock almost doubled rat pineal TV-acetyltransferase activity and the concentrations of melatonin and serotonin. This chapter concentrates on studies of the acute effect of MAO inhibitors on melatonin biosynthesis.

Electroconvulsive therapy is considered to be the most effective treatment for endogenous depression, but despite vigorous research there is no consensus on the mechanism of the antidepressant effect. One attempt to explain the mechanism uses a neuroendocrine hypothesis. Because it is generally accepted that the therapeutic effect of electroconvulsive shock (ECS) occurs after chronic (but not single) administration. In the past decade, evidence accumulated that depression might result from desynchronization of circadian rhythms. Such normalization is achieved simply by a single administration of the pineal gland hormone melatonin in rats. Also, administration of a single dose of melatonin has been reported to change circadian rhythms in humans. Elevation of human plasma melatonin levels was observed after a single dose of the heterocyclic antidepressants, desipramine and fluvoxamine, and of monoamine oxidase (MAO) inhibitors. If the stimulation of melatonin synthesis with consequent normalization of disrupted circadian rhythms is, indeed, the common denominator of the antidepressant effect, it is interesting to study the effect of ECS on melatonin synthesis.

Steroid hormones, including estrogens, play an important role in regulating aggressive behaviors in many vertebrate species. Recent studies have demonstrated that the effects of estrogens on aggressive behaviors are dependent on experience. Studies in the rodent genus Peromyscus indicate that estrogens affect aggressive behavior through different mechanisms under different photoperiod schedules. Under winter-like short days, estrogens were found to act rapidly to increase aggression whereas these rapid effects were absent under long days. In contrast estrogens were found to decrease aggression in mice in long days. Our working hypothesis for these results is that rapid effects of estrogens under short days are mediated by nongenomic pathways whereas the longer term effects of estrogens under long days are mediated by the transcriptional effects of estrogens. These data suggest the molecular pathways downstream of estrogen receptors may be subject to regulation by salient environmental cues such as photoperiod.

This chapter describes the blue moon phenomenon, the effect of anomalous aerosol light scattering, and the red tide and dead fish event caused by dinoflagellate and Gymnodinium brevis. Various studies on rhythmic leaf movements, circadian rhythm, and their control by the endogenous biological clock are presented. The chapter also discusses the incidence of bioluminescence in Gonyaulax polyedra, its mechanism, what causes it, and clock control. The role of melatonin in rhythms, biological rhythm research, and the circadian clock of Gonyaulax and its knowledge and usefulness are emphasized.

This chapter presents an overview of potential maternal effects on behavioral development, including pre- and postnatal effects of social experiences, stress, and seasonality on the expression of developing phenotypes. It suggests that maternal effects will have a selective advantage when they increase the survival and reproductive success of offspring. This chapter also discusses effects of maternal physiology including gonadal hormones, glucocorticoids and melatonin on offspring phenotype.