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• W2073621670 abstract "Prenatal stress (PS) results in a variety of learning, behavioural and emotional alterations observed in later life. Although most human studies exploring the impact of PS on the brain are retrospective and correlational in nature, several lines of evidence link maternal stress to increased basal hypothalamus–pituitary–adrenal (HPA) axis activity in the offspring and disturbances in child development and behaviour, like autism disorder, depression, drug abuse and mood and anxiety disorders (Lupien et al. 2009).During gestation, the maternal neuroendocrine system adopts strategies to cope with stressful experiences and protect the fetus from potentially detrimental programming but some maternal molecular mediators, like glucocorticoids, can cross the placental barrier and exert many organisational effects on prenatal tissue development. In physiological conditions, fetal exposure to maternal glucocorticoids is maintained at a low level by downregulation of the HPA axis and expression of placental enzymes that control the access of glucocorticoids to the fetal compartment. However, a prolonged rise in glucocorticoids and other mediators of PS leads to excessive exposure causing long-term increases in HPA axis activity and downregulates hippocampal receptors that normally aid in the negative feedback to the HPA axis, thereby resulting in a dysregulated axis. Therefore, an uncontrolled increase in basal and/or stress-induced glucocorticoid secretion may cause structural and functional changes within the hippocampus that persist even when glucocorticoid levels return to control values. The time window in which these modifications occur may be critical for development of essential brain functions (Maccari & Morley-Fletcher, 2007).In a recent issue of The Journal of Physiology, Yeh and co-workers (2012) explore the mechanisms underlying alterations of hippocampal synaptic plasticity in rats exposed to PS. Through extracellular electrophysiological recordings in hippocampal slices the authors show that PS affected hippocampal synaptic plasticity early in life but these changes were not maintained into adulthood. In particular in 3- and 5-week-old rats that have been exposed to PS, CA1 long-term potentiation (LTP) amplitude was decreased compared with controls while long-term depression (LTD) was either equally expressed in both control and PS rats (3 weeks) or only in PS-exposed rats (5 weeks). At 8 weeks of age control and PS rats equally expressed LTP but not LTD. The authors then further characterise electrophysiological and morphological aspects and biochemical correlates at this specific time point (5 weeks). While PS did not seem to affect intrinsic properties of CA1 field excitatory postsynaptic potentials, expression of NMDA receptor subunits or dendritic morphology in hippocampal pyramidal neurons, the authors found a positive correlation between increased levels of pro-brain-derived neurotrophic factor (pro-BDNF) vs. mature BDNF (mBDNF) and alterations of synaptic plasticity in PS-exposed rats. PS seems to exert this effect on BDNF subtypes expression by reducing activity and expression of tissue plasminogen activator, which promotes plasmin conversion of pro-BDNF to mBDNF, were markedly reduced.Such results may have important clinical implications since the study finds a time window during development in which behavioural correlates of hippocampal function can be explored to study how synaptic plasticity changes in its BDNF-dependent properties after in utero exposure to stress.mBDNF and pro-BDNF affect neurons positively or negatively through various intracellular signalling pathways, triggered by activation of TrkB and p75 receptors, by stimulating intracellular signalling critical for cell death and proliferation, morphogenesis and plasticity. From a clinical perspective, dysregulation of BDNF expression has been implicated in the pathophysiology of several brain diseases such as epilepsy, autism and depression, and recent studies have investigated possible crosstalk between glucocorticoid- and BDNF/TrkB-mediated signalling in the pathophysiology of depression (Kunugi et al. 2010), further supporting the idea that BDNF expression can be epigenetically modified through generations (Roth & Sweatt, 2011).These findings suggest that the ratio of pro-BDNF/mBDNF could be a critical determinant in the response to PS, opposing or favouring the direction of distinct forms of synaptic plasticity, possibly by inducing changes in the phosphorylation state and/or trafficking of synaptic glutamate receptor subunits primarily involved in the establishment of plastic changes. Along this line, epigenetic modifications induced by PS might perturb the physiological interplay among glutamate, neurotrophic factors and other neurotramsmitter systems in the hippocampus, resulting in a series of maladaptive mechanisms. With time, a damaged hippocampus becomes more susceptible, as a response to stress or metabolic changes may exacerbate pre-existent alterations, creating a downward spiral of increased occasions of damage.Another intriguing aspect that emerges from these data is the distinct expression pattern of plasticity at the three developmental time points. In fact, the authors identified a specific time window in which the effect of PS is more evident, as plasticity is partially altered at 3 weeks (just LTP), completely altered at 5 weeks (both LTP and LTD) and rescued at 8 weeks.Hippocampal BDNF expression alterations occur in in parallel with this pattern, disappearing in adulthood, consistent with studies showing a reduction of BDNF mRNA levels in the prefrontal cortex and striatum of adults prenatally exposed to stress but not in their hippocampus. This suggests that early stress produces anatomically specific effects on BDNF expression.During puberty (beginning at 6 weeks in the rat) steroid hormone actions in the nervous system shape the neuroendocrine system and program a variety of adult habits, by transiently modifying the activity of target cells in ways that facilitate behaviour in specific social contexts but also by permanently organising nervous system structure during development, and this organisational effect is permanent. Therefore, the specific timing of these plastic changes may be critical and predictive of future development of disease, according to recent reports showing PS-induced alteration in grey matter density and learning in children at 6–9 years of age (Sandman et al. 2011). Further studies along this line may open the possibility of therapeutic intervention with positive modulators of BDNF expression in order to limit PS effects in adulthood." @default.
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• W2073621670 date "2012-03-01" @default.
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• W2073621670 title "Prenatal stress and hippocampal BDNF expression: a fading imperative" @default.
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• W2073621670 doi "https://doi.org/10.1113/jphysiol.2012.227777" @default.
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