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The brain-derived neurotrophic factor (BDNF) is involved in the plasticity and development of the central nervous system. Thereby the protein synthesis is highly related to neuronal activity, and its signaling pathways are associated with several substances like, e.g. glucocorticoids, which seem to be able to activate BDNF-Tropomyosin receptor kinase B (TrkB). While there is evidence that acute physical stress can result in advantageous physiological outcomes like an enhanced BDNF level, outcome parameters in response to psychosocial stress are primarily focused on psychological parameters. The existing literature pointing on the impact of acute psychosocial stress on physiological parameters is controversial and differs depending on the species, the stressor used, and the study methodology. It was hypothesized that an acute standardized psychosocial stressor would increase the BDNF level and therefore show beneficial physiological outcome parameters through psychosocial stress. The serum BDNF levels of 32 healthy young males (M = 24.31 years of age, SD = 3.35), who performed the Trier Social Stress Test (TSST), were assessed and compared to a control condition. To prove the stress-generating effect of the TSST, additional cortisol levels were measured. Acute psychosocial stress significantly increased the serum BDNF- and the cortisol-level, whereby no alteration was found during the control. This study expands the rare literature focusing on the effect of an acute standardized psychosocial stressor on the BDNF level in healthy humans, including a control condition. Implications for future studies are being discussed. [ABSTRACT FROM AUTHOR]

Monoamine metabolism in the central nervous system is altered by dietary iron deficiency, with a stronger effect seen during the active than rest span of the circadian cycle. In this report, we examined changes in intracellular and extracellular monoamine levels, synthetic enzymes, transporter and receptor densities, and responses to amphetamine-induced dopamine (DA) efflux in iron-deficient and iron-sufficient mice. Extracellular striatal DA levels were 15-20% higher in all groups during the active dark phase compared to the inactive light phase, with correspondingly lower dopamine transporter (DAT) and higher tyrosine hydroxylase levels. Iron deficiency decreased DAT density by 20% and 28% in the light and dark phases, respectively, and elevated the DOPAC/DA ratio only in the dark, indicating that iron deficiency does interact with the normal diurnal cues for cyclicity. Enhanced DA efflux after amphetamine stimulation indicates no limitation on monoamine synthesis and release and is consistent with altered synaptic efficacy and perhaps recycling of DA in iron deficiency. These experimental findings provide new evidence that brain iron insufficiency does have a differential effect on the DA system at different biological times of the day and night and may be causally related to the phasic motor symptoms observed in Restless Legs Syndrome. [ABSTRACT FROM AUTHOR]