We then specify definitions
that maximise international comparability. Even with this optimisation of data usage, only seven of the 25 indicators, covered at least 50% of the world’s adolescents. The worst adolescent health profiles are in sub-Saharan Dinaciclib Africa, with persisting high mortality from maternal and infectious causes. Risks for non-communicable diseases are spreading rapidly, with the highest rates of tobacco use and overweight, and lowest rates of physical activity, predominantly in adolescents living in low-income and middle-income countries. Even for present global health agendas, such as HIV infection and maternal mortality, data sources are incomplete for adolescents. We propose a series of steps that include better coordination and use of data collected across countries, greater harmonisation of school-based surveys, further development of strategies for socially marginalised youth, targeted research into the validity
and use of these health indicators, advocating for adolescent-health information within new global health initiatives, and a recommendation that every country produce a regular report on the health of its adolescents.”
“Agomelatine is a melatonergic MT1/MT2 agonist and a serotonin (5-HT) 5-HT2C antagonist. The effects of 2-day and 14-day administration of agomelatine were investigated on the activity of ventral tegmental area (VTA) dopamine (DA), locus coeruleus (LC) norepinephrine (NE), and dorsal raphe nucleus (DRN) 5-HT neurons using in vivo electrophysiology in rats. The 5-HT1A transmission was assessed at hippocampus CA3 pyramidal neurons. Dorsomorphin cell line After a 2-day regimen of agomelatine (40 mg/kg/day, i.p.), an increase in the number of spontaneously active VTA-DA neurons (p < 0.001) and in the firing rate of LC-NE neurons (p < 0.001) was observed. After 14 days, the administration of agomelatine induced an increase in: (1) the number of spontaneously active DA neurons (p < 0.05), (2) the Sitaxentan bursting activity of DA neurons (bursts/min, p < 0.01 and percentage of spikes
occurring in bursts, p < 0.05), (3) the firing rate of DRN-5-HT neurons (p < 0.05), and (4) the tonic activation of postsynaptic 5-HT1A receptors located in the hippocampus. The increase in 5-HT firing rate was D2 dependent, as it was antagonized by the D2 receptor antagonist paliperidone. The enhancement of NE firing was restored by the 5-HT2A receptor antagonist MDL-100,907 after the 14-day regimen. All the effects of agomelatine were antagonized by a single administration of the melatonergic antagonist S22153 (except for the increase in the percentage of spikes occurring in burst for DA neurons). The present results suggest that (1) agomelatine exerts direct (2 days) and indirect (14 days) modulations of monoaminergic neuronal activity and (2) the melatonergic agonistic activity of agomelatine contributes to the enhancement of DA and 5-HT neurotransmission. Neuropsychopharmacology (2013) 38, 275-284; doi:10.1038/npp.2012.