Brain derived neutrophic factor, a link of aerobic metabolism to neuroplasticity.

Currently, literature has accumulated great knowledge over the effect of exercise on the neurotrophin named brain derived neurotrophic factor (BDNF) and its role in neuronal plasticity. However, there is no enough discussion about how the exercise is related to enrichment of BDNF in specific metabolic properties. This review provides the current evidences regarding aerobic metabolism relation to BDNF concentrations in healthy individuals. A PICOS strategy was applied considering the mesh terms for: P - healthy subjects; I - physical exercise; C - aerobic metabolism demands; O - BDNF concentrations; S - before and after aerobic exercise; on PubMed, Scopus and Medline databases. Studies presenting at least one session the exercise with reports of BDNF analysis before and after were included. Reviews, letters, case-reports, articles not written in English, non- published or involving non-healthy populations were excluded. Compiling results, it was possible to observe a close interaction between different aerobic energy demands from the exercise models and the responses of BDNF, suggesting thus that increases in BDNF concentrations are associated to the amount of aerobic energy required by exercise in a dose-dependent manner. Moreover, the dynamics of BDNF synthesis and reuptake resemble the functioning of the metabolic systems of aerobic energy generation, with which they share a co-transcriptional factor dependence.

Novel aspects of glucocorticoid actions.

Normal hypothalamic-pituitary-adrenal (HPA) axis activity leading to the rhythmic and episodic release of adrenal glucocorticoids (GCs) is essential for body homeostasis and survival during stress. Acting through specific intracellular receptors in the brain and periphery, GCs regulate behaviour, as well as metabolic, cardiovascular, immune and neuroendocrine activities. By contrast to chronic elevated levels, circadian and acute stress-induced increases in GCs are necessary for hippocampal neuronal survival and memory acquisition and consolidation, as a result of the inhibition of apoptosis, the facilitation of glutamatergic neurotransmission and the formation of excitatory synapses, and the induction of immediate early genes and dendritic spine formation. In addition to metabolic actions leading to increased energy availability, GCs have profound effects on feeding behaviour, mainly via the modulation of orexigenic and anorixegenic neuropeptides. Evidence is also emerging that, in addition to the recognised immune suppressive actions of GCs by counteracting adrenergic pro-inflammatory actions, circadian elevations have priming effects in the immune system, potentiating acute defensive responses. In addition, negative-feedback by GCs involves multiple mechanisms leading to limited HPA axis activation and prevention of the deleterious effects of excessive GC production. Adequate GC secretion to meet body demands is tightly regulated by a complex neural circuitry controlling hypothalamic corticotrophin-releasing hormone (CRH) and vasopressin secretion, which are the main regulators of pituitary adrenocorticotrophic hormone (ACTH). Rapid feedback mechanisms, likely involving nongenomic actions of GCs, mediate the immediate inhibition of hypothalamic CRH and ACTH secretion, whereas intermediate and delayed mechanisms mediated by genomic actions involve the modulation of limbic circuitry and peripheral metabolic messengers. Consistent with their key adaptive roles, HPA axis components are evolutionarily conserved, being present in the earliest vertebrates. An understanding of these basic mechanisms may lead to novel approaches for the development of diagnostic and therapeutic tools for disorders related to stress and alterations of GC secretion.