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Borbely AA, Achermann P. Sleep homeostasis and models of sleep regulation. In: Kryger MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine. Philadelphia: Elsevier Saunders; 2005. p. 405–17.
Why is adolescence in polyphasic animal species accompanied by a phase advance in puberty? What is the function of a phase delay during adolescence in humans? The effects of sleep on performance are conveyed primarily during non-REM sleep. In adults, slow oscillations in particular are thought to be actively involved in cortical plastic processes associated with learning [ 77•, 78, 79]. During vulnerable periods of life, sleep may be important for plastic processes associated with neurodevelopment (see also the next paragraph). Epidemiological studies show that disturbed sleep throughout preschool and the school age years is associated with psychosocial, somatic, and medical problems [ 80]. Moreover, sleep problems in childhood predict later psychological and social problems over and above demographic factors [ 81]. While REM sleep might be of importance for performance benefits during early cortical development [ 82], SWA during non-REM sleep was suggested to contribute to reorganization processes in synaptic connections at a later age [ 83]. Human studies concerning the involvement of sleep in neuroplasticity during development, however, remain correlative. Taveras EM, Rifas-Shiman SL, Oken E, Gunderson EP, Gillman MW. Short sleep duration in infancy and risk of childhood overweight. Arch Pediatr Adolesc Med. 2008;162(4):305–11.Ringli M, Huber R. Developmental aspects of sleep slow waves: linking sleep, brain maturation and behavior. Prog Brain Res. 2011;193:63–82.
The human cortex matures in a posterior-to-anterior trajectory, as measured with both MRI-derived gray matter volumes [ 45] and SWA topography assessed with high-density EEG [ 38]. Likewise, in other primates, dendrites of prefrontal pyramidal neurons develop later than sensorimotor areas [ 42]. In rats, the primary motor cortex also matures earlier in comparison to the visual cortex, which receives sensory input only after eye opening after P14 [ 46]. White Matter Development Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342(6156):373–7. Frank MG, Morrissette R, Heller HC. Effects of sleep deprivation in neonatal rats. Am J Physiol. 1998;275(1 Pt 2):R148–57. Jha SK, Jones BE, Coleman T, Steinmetz N, Law CT, Griffin G, et al. Sleep-dependent plasticity requires cortical activity. J Neurosci: Off J Soc Neurosci. 2005;25(40):9266–74.Diclofenac is completely absorbed from the GI tract but likely undergoes significant first pass metabolism with only 60% of the drug reaching systemic circulation unchanged . Many topical formulations are absorbed percutaneous and produce clinically significant plasma concentrations. Absorption is dose proportional over the range of 25-150 mg. Tmax varies between formulations with the oral solution reaching peak plasma concentrations in 10-40min, the enteric coated tablet in 1.5-2h, and the sustained- and extended-release formulations prolonging Tmax even further. Administration with food has no significant effects on AUC but does delay Tmax to 2.5-12h. Sleep is ubiquitously found in the animal kingdom, yet its core functions are unknown. Sleep possibly serves various functions, and the proposed hypotheses may be summarized into three main categories: First, sleep serves to reduce energy expenditure; second, sleep is needed for the restoration of key cellular components and macromolecule biosynthesis; and third, sleep facilitates learning and memory by means of improved function based on synaptic plasticity processes [ 75]. We discuss specific aspects of these theories in the context of neurodevelopmental changes in the subsequent paragraphs. Sleep Is Important for Balancing Synaptic Strength Hypothesis: Touchette E, Cote SM, Petit D, Liu X, Boivin M, Falissard B, et al. Short nighttime sleep-duration and hyperactivity trajectories in early childhood. Pediatrics. 2009;124(5):e985–93. Diclofenac inhibits cyclooxygenase-1 and -2, the enzymes responsible for production of prostaglandin (PG) G 2 which is the precursor to other PGs. These molecules have broad activity in pain and inflammation and the inhibition of their production is the common mechanism linking each effect of diclofenac. Fields RD. Imaging learning: the search for a memory trace. Neuroscientist : Rev J Bringing Neurobiol Neurol Psychiatry. 2011;17(2):185–96.
Buchmann A, Ringli M, Kurth S, Schaerer M, Geiger A, Jenni OG, et al. EEG sleep slow-wave activity as a mirror of cortical maturation. Cereb Cortex. 2011;21(3):607–15. Jenni OG, Borbely AA, Achermann P. Development of the nocturnal sleep electroencephalogram in human infants. Am J Physiol Regul Integr Comp Physiol. 2004;286(3):R528–38. Symptoms of overdose include lethargy, drowsiness, nausea, vomiting, and epigastric pain, and gastrointestinal bleeding. Hypertension, acute renal failure, respiratory depression and coma occur rarely. In case of overdose, provide supportive care and consider inducing emesis and administering activated charcoal if overdose occurred less than 4 hours prior.Wieraszko A. Changes in the hippocampal slices energy metabolism following stimulation and long-term potentiation of Schaffer collaterals-pyramidal cell synapses tested with the 2-deoxyglucose technique. Brain Res. 1982;237(2):449–57. Grains [cereals]; Bran; Seeds for planting; Raw and unprocessed seeds; Vegetable seeds; Seeds for fruit. In concert with cortical gray matter growth during childhood, underlying axonal bundles become progressively myelinated (see [ 47] for quantitative analyses or [ 48] for a review). In all mammalian species, the formation of myelin sheaths is essential for the propagation and speed of neurotransmission. Oligodendrocytes wrap axons with myelin, consisting of multiple layers of closely opposed glial membranes. This insulation improves the passive flow of electrical current, resulting in up to a 1000-fold increase in action potential conduction speed.
Lenroot RK, Giedd JN. Brain development in children and adolescents: insights from anatomical magnetic resonance imaging. Neurosci Biobehav Rev. 2006;30(6):718–29. Khazipov R, Esclapez M, Caillard O, Bernard C, Khalilov I, Tyzio R, et al. Early development of neuronal activity in the primate hippocampus in utero. J Neurosci: Off J Soc Neurosci. 2001;21(24):9770–81. The main trademark of cortical development is a combination of expansion and regression. The number of synapses in children exceeds adult levels [ 34], as many more synaptic connections are produced than will finally be retained [ 35]. Neuronal refinement includes the removal of neurons and synapses that fail to make appropriate connections, which ensures the establishment of proper connectivity [ 36]. Although such regressive processes are most frequent during brain development in early life, they continue to a lesser extent throughout the first two decades of life. Tarokh L, Carskadon MA, Achermann P. Developmental changes in brain connectivity assessed using the sleep EEG. Neuroscience. 2010;171(2):622–34.
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Bianchi S, Stimpson CD, Duka T, Larsen MD, Janssen WG, Collins Z, et al. Synaptogenesis and development of pyramidal neuron dendritic morphology in the chimpanzee neocortex resembles humans. Proc Natl Acad Sci U S A. 2013;110 Suppl 2:10395–401. Vyazovskiy VV, Cirelli C, Pfister-Genskow M, Faraguna U, Tononi G. Molecular and electrophysiological evidence for net synaptic potentiation in wake and depression in sleep. Nat Neurosci. 2008;11(2):200–8.
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