More Than Just an OFF-Switch: The Essential Role of Protein Dephosphorylation in the Modulation of BDNF Signaling Events

Deinhardt, Katrin; Jeanneteau, Freddy

doi:10.5772/50420

Cited by 3 publications

(2 citation statements)

References 59 publications

(60 reference statements)

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“…Binding of BDNF to TrkB triggers different signaling cascades, some of which regulate protein translation and transport (mitogen-activated protein kinase MAPK, and phosphatidylinositol 3-kinase PI3K), whereas others regulate the intracellular release of calcium in postsynaptic sites (phospholipase Cγ, PLCγ) [ 18 ]. These downstream signaling pathways are initiated by the binding of BDNF to TrkB and autophosporylation of tyrosine residues including Y817, which serves as docking sites for effector proteins in the intracellular domain [ 19 , 20 ]. Thus, assessing the effects on BDNF, TrkB, and Y817 provides information on the potentially involved regulatory pathways as well as the putative biological significance (i.e., active vs. inactive forms).…”

Section: Introductionmentioning

confidence: 99%

A Long-Term Energy-Rich Diet Increases Prefrontal BDNF in Sprague-Dawley Rats

et al. 2021

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Findings of the effect of high-fat feeding including “Cafeteria Diets” (CAF) on brain-derived neurotrophic factor (BDNF) in the hippocampus (HIP) and prefrontal cortex (PFC) in rodents are conflicting. CAF is a non-standardized, highly palatable energy-rich diet composed by everyday food items for human consumption and is known to induce metabolic syndrome and obesity in rats. However, the highly palatable nature of CAF may counteract a negative effect of chronic stress on anticipatory behavior and synaptic plasticity in the hippocampus, hence represent a confounding factor (e.g., when evaluating functional effects on the brain). This study investigated the effects of a chronic, restricted access to CAF on BDNF, monoamine neurotransmitters, and redox imbalance in HIP and PFC in male rats. Our results show that CAF induced BDNF and its receptor TrkB in PFC compared to the controls (p < 0.0005). No differences in monoamine neurotransmitters were detected in either PFC or HIP. CAF increased dehydroascorbic acid and decreased malondialdehyde in PFC (p < 0.05), suggesting an early redox imbalance insufficient to induce lipid peroxidation. This study supports that a chronic CAF on a restricted schedule increases BDNF levels in the PFC of rats, highlighting that this may be a suboptimal feeding regime when investigating the effects of diet-induced obesity in the brain and emphasizing this as a point of attention when comparing the findings.

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Section: Introductionmentioning

confidence: 99%

A Long-Term Energy-Rich Diet Increases Prefrontal BDNF in Sprague-Dawley Rats

et al. 2021

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“…Mechanisms of adaptive plasticity utilize immediate early genes as first line responders to glucocorticoid stimulation to prepare cells for a changing environment based on prior experience. For example, the MAPK specific phosphatases (Mitogen-Activated Protein Kinase Phosphatase 1/6 [MKP1/6]) are induced to terminate coincident growth factor signaling pathways converging on the GR phosphorylation code and the epigenome (Deinhardt and Jeanneteau, 2012;Jeanneteau and Deinhardt, 2011). Another example is the stress-induced transcription factors NR4A1/2/3, which shuttle in and out of the nucleus and mitochondria to coordinate metabolism and synapses number (Jeanneteau et al, 2018).…”

Section: At the Single Cell Levelmentioning

confidence: 99%

Experience and activity-dependent control of glucocorticoid receptors during the stress response in large-scale brain networks

Huzard

Rappeneau

Meijer

et al. 2020

Stress

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The diversity of actions of the glucocorticoid stress hormones among individuals and within organs, tissues and cells is shaped by age, gender, genetics, metabolism, and the quantity of exposure. However, such factors cannot explain the heterogeneity of responses in the brain within cells of the same lineage, or similar tissue environment, or in the same individual. Here, we argue that the stress response is continuously updated by synchronized neural activity on large-scale brain networks. This occurs at the molecular, cellular and behavioral levels by crosstalk communication between activity-dependent and glucocorticoid signaling pathways, which updates the diversity of responses based on prior experience. Such a Bayesian process determines adaptation to the demands of the body and external world. We propose a framework for understanding how the diversity of glucocorticoid actions throughout brain networks is essential for supporting optimal health, while its disruption may contribute to the pathophysiology of stress-related disorders, such as major depression, and resistance to therapeutic treatments.

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Antidepressant-like effects of rosmarinic acid through mitogen-activated protein kinase phosphatase-1 and brain-derived neurotrophic factor modulation

Kondo

Omri

Han

et al. 2015

Journal of Functional Foods

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21Rosmarinic acid (RA) is one of the major bioactive compounds of Rosmarinus officinalis, a 22 culinary and edible aromatic plant and was demonstrated to have several neuroprotective 23 properties including anti-depressive-like effect. The current study was designed to contribute 24 to understanding the molecular mechanism of RA beneficial effects in tail suspension test 25 (TST)-induced depression in mice with bupropion as positive control, and mice without TST 26 as negative control. Changes in serum corticosterone (CORT) level and cerebrum level of 27 catecholamines: dopamine (DOP), noradrenaline (NAD), and adrenaline (ADR) were 28 investigated. Moreover, brain-derived neutrophic factor (Bdnf), mitogen-activated protein 29 kinase phosphatase-1 (Mkp-1), tyrosine hydroxylase (Th) and pyruvate carboxylase (Pc) gene 30 expression in mice cerebrum were investigated using real-time PCR. RA was demonstrated to 31 show anti-depressant-like effect by significant reduction of immobility time in the TST in 32 mice. This effect was accompanied by a downregulation of Mkp-1 to reach the unstressed 33 group level, an upregulation of Bdnf, Th and Pc in the limbic system. Furthermore, RA 34 significantly decreased serum corticosterone level and increased dopamine level in the limbic 35 system in mice brain.Our study provides the first evidence that RA has anti-depressant activity 36 via downregulation of Mkp-1, upregulation of Bdnf and modulation of dopamine and 37 corticosterone synthesis.38 39

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More Than Just an OFF-Switch: The Essential Role of Protein Dephosphorylation in the Modulation of BDNF Signaling Events

Cited by 3 publications

References 59 publications

A Long-Term Energy-Rich Diet Increases Prefrontal BDNF in Sprague-Dawley Rats

A Long-Term Energy-Rich Diet Increases Prefrontal BDNF in Sprague-Dawley Rats

Experience and activity-dependent control of glucocorticoid receptors during the stress response in large-scale brain networks

Antidepressant-like effects of rosmarinic acid through mitogen-activated protein kinase phosphatase-1 and brain-derived neurotrophic factor modulation

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