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The Biological Basis of Non-Image-Forming Vision
Published in Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe, Visual and Non-Visual Effects of Light, 2020
Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe
The M1 subtype of ipRGCs project to many regions in the brain, showing their functional involvement: in the suprachiasmatic nucleus (SCN), the master circadian clock,in the intergeniculate leaflet (IGL), a center for circadian entrainment, integration of photic and nonphotic circadian cues,in the shell of olivary pretectal nucleus (OPN), a center for the pupillary light reflex,in the ventral subparaventricular zone (vSPZ), implicated in acute arrest of locomotor activity by light in nocturnal animals,in the posterior thalamic nucleus, dorsal border, nociception,in the ventrolateral preoptic nucleus (VLPO), a control center for sleep,in the medial amygdala,in the lateral habenula (integration of the limbic, motor, and circadian systems).
Neuroscience of Sleep and Circadian Rhythms
Published in Gerald Matthews, Paula A. Desmond, Catherine Neubauer, P.A. Hancock, The Handbook of Operator Fatigue, 2017
Siobhan Banks, Melinda L. Jackson, Hans P.A. Van Dongen
Waking alertness is sustained by the combined action of various wake-promoting centers in the brain (e.g., reticular activating system, locus coeruleus and tuberomammillary nucleus), which utilize monoaminergic (serotonin, dopamine, histamine, adrenalin, noradrenalin) and cholinergic neurotransmitters to promote neuronal activation (Saper, Chou & Scammell, 2001; see Figure 11.1). A brain area called the ventrolateral preoptic nucleus (VLPO) monitors the sleep propensity state of the brain (possibly via detection of increases in extracellular ATP; Krueger et al., 2010) and triggers whole-brain sleep when sleep propensity becomes excessive. The VLPO blocks the activity of wake-promoting centers in the brain (such as the locus coeruleus and tuberomammillary nucleus) through the inhibitory neurotransmitter GABA, and thereby promotes sleep (Fuller, Gooley & Saper, 2006).
Identification and Prediction of Substantial Differential Vulnerability to the Neurobehavioral Effects of Sleep Loss
Published in Steven Kornguth, Rebecca Steinberg, Michael D. Matthews, Neurocognitive and Physiological Factors During High-Tempo Operations, 2018
The stability of wakefulness and the consolidation of sleep are controlled by a set of complex neural pathways. There is currently no singular unifying theory describing their interactions, although their neurobehavioral outputs and effects on neurobehavioral functions are increasingly predictable through mathematical models of these processes (McCauley et al. 2009). The ascending cholinergic reticulothalamocortical pathway, which originates in the upper pons, pedunculopontine, and lateral dorsal tegmental nuclei, and activates the thalamus and cerebral cortex, has a major role in maintaining arousal and wakefulness, although histaminergic, noradrenergic, dopaminergic, and serotonergic mechanisms likely also play a role. Conversely, the ventrolateral preoptic nucleus (VLPO), an area rich in galanin- and GABA-containing neurons, is active during sleep, and is a highly accurate real-time marker of sleep duration. The ascending cholinergic pathway and VLPO are mutually inhibitory, thus forming a “flip-flop” switch that when activated tends to stay active by inhibiting the opposing pathway (Saper et al. 2005). A small perturbation in the system may lead to a sudden change in the pathway whose activity is dominant (for example, instability can occur under certain conditions). There is also evidence that orexin-hypocretin neurons are responsible for both stabilizing the sleep switch and altering its equilibrium point (from promoting wakefulness to promoting sleep and vice versa). These molecules interact directly with the arousal system, but not with the VLPO, suggesting that their action inhibits unwanted lapses into sleep (Mignot 2004). Adenosinergic mechanisms also likely participate in the regulation of sleep homeostasis (Porkka-Heiskanen et al. 2000, Strecker et al. 2000), and the output of the suprachiasmatic nuclei (the endogenous circadian clock) modulates the stability of waking neurobehavioral functions.
A computational model of pupil dilation
Published in Connection Science, 2018
Birger Johansson, Christian Balkenius
In addition, several parts of the hypothalamus, like the Ventrolateral Preoptic Nucleus (VPLO), which is involved in sleep regulation, and the suprachiasmatic nucleus (SCN) and the dorsomedial nucleus (DMH), that are involved in circadian rhythms, can influence the pupil through LC. There is also a light controlled path from the retina to the SCN that inhibits the paraventricular nucleus (PVN), which in turn connects with the sympathetic system. We do not address the effects of these hypothalamic nuclei here.