Correlations and Discrepancies between Serum and Brain Tissue Levels of Neurotrophins after Electroconvulsive Treatment in Rats

Sartorius, Alexander; Hellweg, Rainer; Litzke, Julia Ulrike; Vogt, Miriam A.; Dormann, Christof; Vollmayr, Barbara; Danker‐Hopfe, Heidi; Gass, Peter

doi:10.1055/s-0029-1224162

Cited by 257 publications

(148 citation statements)

References 44 publications

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“…68,69 There is evidence that peripheral NF concentrations are associated with brain tissue expression. 70 Indeed, cerebral BDNF crosses the blood-brain barrier, and it has been suggested that peripheral BDNF levels are correlated with brain tissue BDNF levels in rodents. 70 Moreover NGF, NT3, and NT-4/5 can cross the blood-brain barrier of mice in vivo to arrive at the brain parenchyma, and peripheral administration of neurotrophins could have neurobiological effects within the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

“…70 Indeed, cerebral BDNF crosses the blood-brain barrier, and it has been suggested that peripheral BDNF levels are correlated with brain tissue BDNF levels in rodents. 70 Moreover NGF, NT3, and NT-4/5 can cross the blood-brain barrier of mice in vivo to arrive at the brain parenchyma, and peripheral administration of neurotrophins could have neurobiological effects within the central nervous system. 71 However, plasma BDNF has been hypothesized to behave as a state-dependent marker, while serum BDNF might signify illness.…”

Section: Discussionmentioning

confidence: 99%

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Neurotrophic factors in women with crack cocaine dependence during early abstinence: the role of early life stress

Viola

Tractenberg

Levandowski

et al. 2014

J Psychiatry Neurosci

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neurotrophic factors in women with crack cocaine dependence during early abstinence: the role of early life stress

Viola

Tractenberg

Levandowski

et al. 2014

J Psychiatry Neurosci

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“…Moreover, the strong correlation between decreases in serum BDNF concentration and changes in neuroplasticity strongly suggests that serum BDNF concentration reflects the presence of residual traces responsible for vulnerability to depression. Although the mechanisms allowing us to explain the relationship between serum and hippocampal BDNF are unknown, a recent study showed that measuring serum BDNF concentration can be used to monitor changes in neurotrophin levels in brain tissue (Sartorius et al, 2009). A decrease in serum BDNF concentration associated with normal serum cortisol concentration may be considered a relevant biomarker for identifying, within a population at risk, individuals more likely to develop depressive disorders.…”

Section: Discussionmentioning

confidence: 99%

Vulnerability to Depression: From Brain Neuroplasticity to Identification of Biomarkers

Blugeot¹,

Rivat²,

Bouvier³

et al. 2011

J. Neurosci.

161

147

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A stressful event increases the risk of developing depression later in life, but the possible predisposing factors remain unknown. Our study aims to characterize latent vulnerability traits underlying the development of depressive disorders in adult animals. Four weeks after a priming stressful event, serum corticosterone concentration returned to control values in all animals, whereas the other biological parameters returned to basal level in only 58% of animals (called nonvulnerable). In contrast, 42% of animals displayed persistent decreased serum and hippocampus BDNF concentrations, reduced hippocampal volume and neurogenesis, CA3 dendritic retraction and decrease in spine density, as well as amygdala neuron hypertrophy, constituting latent vulnerability traits to depression. In this group, called vulnerable, a subsequent mild stress evoked a rise of serum corticosterone levels and a "depressive" phenotype, in contrast to nonvulnerable animals. Intracerebroventricular administration of 7,8-dihydroxyflavone, a selective TrkB receptor agonist, dampened the development of the "depressive" phenotype. Our results thus characterize the presence of latent vulnerability traits that underlie the emergence of depression and identify the association of low BDNF with normal corticosterone serum concentrations as a predictive biomarker of vulnerability to depression.

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“…In support of this, BDNF can readily cross the blood-brain barrier via a high-capacity transport system (Pan et al, 1998;Poduslo and Curran, 1996), serum BDNF correlates with cortical BDNF mRNA expression (Gervasoni et al, 2005), and serum BDNF may be affected by changes in cortical BDNF. For example, electroconvulsive treatments result in increased cortical BDNF followed by a rise in serum BDNF (Sartorius et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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Depression has been associated with inflammation, and inflammation may both influence and interact with growth factors such as brainderived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) and BDNF levels have been associated with depression. It is thus plausible that decreased BDNF could mediate and/or moderate cytokine-induced depression. We therefore prospectively employed the Beck Depression Inventory-II (BDI-II), the Hospital Anxiety and Depression Scale (HADS), and the Montgomery-Asberg Depression Rating Scale (MADRS) in 124 initially euthymic patients during treatment with interferon-alpha (IFN-a), assessing serum BDNF and rs6265. Using mixed-effect repeated measures, lower pretreatment BDNF was associated with higher depression symptoms during IFN-a treatment (F 144,17.2 ¼ 6.8; Po0.0001). However, although the Met allele was associated with lower BDNF levels (F 1,83.0 ¼ 5.0; P ¼ 0.03), it was only associated with increased MADRS scores (F 4,8.9 ¼ 20.3; Po0.001), and not the BDI-II or HADS. An exploratory comparison of individual BDI-II items indicated that the Met allele was associated with suicidal ideation, sadness, and worthlessness, but not neurovegetative symptoms. Conversely, the serotonin transporter promoter polymorphism (5-HTTLPR) short allele was associated with neurovegetative symptoms such as insomnia, poor appetite and fatigue, but not sadness, worthlessness, or suicidal ideation. IFN-a therapy further lowered BDNF serum levels (F 4,37.7 ¼ 5.0; P ¼ 0.003), but this decrease occurred regardless of depression development. The findings thus do not support the hypothesis that decreasing BDNF is the primary pathway by which IFN-a worsens depression. Nonetheless, the results support the hypothesis that BDNF levels influence resiliency against developing inflammatory cytokine-associated depression, and specifically to a subset of symptoms distinct from those influenced by 5-HTTLPR. Neuropsychopharmacology (2013) 38, 985-995;

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Correlations and Discrepancies between Serum and Brain Tissue Levels of Neurotrophins after Electroconvulsive Treatment in Rats

Abstract: The time course of central and peripheral BDNF changes may significantly differ. However, we demonstrate substantial evidence that it can be justified to measure serum BDNF levels with a time delay to monitor brain tissue neurotrophin alterations.

Cited by 257 publications

References 44 publications

Neurotrophic factors in women with crack cocaine dependence during early abstinence: the role of early life stress

Neurotrophic factors in women with crack cocaine dependence during early abstinence: the role of early life stress

Vulnerability to Depression: From Brain Neuroplasticity to Identification of Biomarkers

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

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