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We will then discuss the behavioral functions of BNST-hypothalamus circuitry, including valence surveillance, addiction, feeding, and social behavior. Finally, we will address sex differences in morphology and function of the BNST and hypothalamus.The bed nucleus of the stria terminalis (BNST) is a compact but neurophenotypically complex structure in the ventral forebrain that is structurally and functionally linked to other limbic structures, including the amygdala nuclear complex, hypothalamic nuclei, hippocampus, and related midbrain structures, to participate in a wide range of functions, especially emotion, emotional learning, stress-related responses, and sexual behaviors. From a variety of sensory inputs, the BNST acts as a node for signal integration and coordination for information relay to downstream central neuroendocrine and autonomic centers for appropriate homeostatic physiological and behavioral responses. In contrast to the role of the amygdala in fear, the BNST has gained wide interest from work suggesting that it has main roles in mediating sustained responses to diffuse, unpredictable and/or long-duration threats that are typically associated with anxiety-related responses. Further, some BNST subregions are highly sexually dimorphic circuit interactions.Antipsychotic drugs are efficacious first-line treatments for many individuals diagnosed with a psychiatric illness. However, their adverse metabolic side-effect profile, which resembles the metabolic syndrome, represents a significant clinical problem that increases morbidity and limits treatment adherence. Moreover, the mechanisms involved in antipsychotic-induced adverse metabolic effects (AMEs) are unknown and mitigating strategies and interventions are limited. However, recent clinical trials show that nightly administration of exogenous melatonin may mitigate or even prevent antipsychotic-induced AMEs. This clinical evidence in combination with recent preclinical data implicate the circadian system in antipsychotic-induced AMEs and their mitigation. In this chapter, we provide an overview on the circadian system and its involvement in antipsychotic-induced AMEs, as well as the potential beneficial effect of nightly melatonin administration to mitigate them.The objective of chronotherapy is to optimize medical treatments taking into account the body's circadian rhythms. Chronotherapy is referred to and practiced in two different ways (1) to alter the sleep-wake rhythms of patients to improve the sequels of several pathologies; (2) to take into account the circadian rhythms of patients to improve therapeutics. Even minor dysfunction of the biological clock can greatly affect sleep/wake physiology causing excessive diurnal somnolence, increase in sleep onset latency, phase delays or advances in sleep onset, frequent night awakenings, reduced sleep efficiency, delayed and shortened rapid eye movement sleep, or increased periodic leg movements. Chronotherapy aims to restore the proper circadian pattern of the sleep-wake cycle, through adequate sleep hygiene, timed light exposure, and the use of chronobiotic medications, such as melatonin, that affect the output phase of circadian rhythms, thus controlling the clock. Concerning the second use of chronotherapy, therapeutic outcomes as diverse as the survival after open-heart surgery or the efficacy and tolerance to chemotherapy vary according to the time of day. However, humans are heterogeneous concerning the timing of their internal clocks. Not only different chronotypes exist but also the endogenous human circadian period (τ) is not a stable trait as it depends on many internal and external factors. If any scheduled therapeutic intervention is going to be optimized, a tool is needed for simple diagnostic and objectively measurement of an individual's internal time at any given time. Methodologic advances like the use of single-sample gene expression and metabolomics are discussed.In mammals, including humans, the neurohormone melatonin is mainly secreted from the pineal gland at night and acts on two high-affinity G protein-coupled receptors, the melatonin MT1 and MT2 receptors. Major functions of melatonin receptors in the brain are the regulation of circadian rhythms and sleep. Correspondingly, the main indications of the currently available drugs for these receptors indicate this as targets. Yet these drugs may not only improve circadian rhythm- and sleep-related disorders but may also be beneficial for complex diseases like major depression, Alzheimer's disease, autism, and attention-deficit/hyperactivity disorders. Here, we will focus on the hypothalamic functions of melatonin receptors by updating our knowledge on their hypothalamic expression pattern at normal, aged, and disease states, by discussing their capacity to regulate circadian rhythms and sleep and by presenting the clinical applications of the melatonin receptor-targeting drugs ramelteon, tasimelteon, and agomelatine or of prolonged-release melatonin formulations. Finally, we speculate about future trends in the field of melatonin receptor drugs.Melatonin (MLT), secreted during the night by the pineal gland, is an efferent hormonal signal of the master circadian clock located in the suprachiasmatic nucleus (SCN). Consequently, it is a reliable phase marker of the SCN clock. If one defines as "chronobiotic," a drug able to influence the phase and/or the period of the circadian clock, MLT is a very potent one. The most convincing data obtained so far come from studies on totally blind individuals. Exogenous MLT administered daily entrains the sleep-wake cycle of these individuals to a 24-h cycle. MLT, however, is not essential to sleep. In nocturnally, active mammals, MLT is released during the night concomitantly with the daily period of wakefulness. Therefore, MLT cannot be simply considered as a sleep hormone, but rather as a signal of darkness. Its role in the circadian system is to reinforce nighttime physiology, including timing of the sleep-wake cycle and other circadian rhythms. this website MLT exerts its effects on the sleep cycle especially by a direct action on the master circadian clock.