Pre- and postsynaptic twists in BDNF secretion and action in synaptic plasticity

Edelmann, Elke; Leßmann, Volkmar; Brigadski, Tanja

doi:10.1016/j.neuropharm.2013.05.043

Cited by 216 publications

(193 citation statements)

References 242 publications

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“…In addition, considering the involvement of BDNF in synaptic plasticity (Edelmann, Leßmann, & Brigadski, 2013), it is possible that variation in the BDNF gene affects a biological sensitivity to environmental cues more generally. Even though we demonstrated that an interaction between fathers’ BDNF genotype and child conduct problems did not predict paternal warmth, it is possible that fathers with the Met allele will react by adapting a different parental behavior, such as harsh discipline or love withdrawal, in accordance with the child's level of conduct problems.…”

Section: Discussionmentioning

confidence: 99%

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

Avinun

Knafo‐Noam

2017

Brain and Behavior

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BackgroundParental warmth has been associated with various child behaviors, from effortful control to callous‐unemotional traits. Factors that have been shown to affect parental warmth include heritability and child behavior. However, there is limited knowledge about which specific genes are involved, how they interact with child behavior, how they affect differential parenting, and how they affect fathers. We examined what affects paternal and maternal warmth by focusing on the child's prosocial behavior and parents’ genotype, specifically a Valine to Methionine substitution at codon 66 in the brain‐derived neurotrophic factor (BDNF) gene.MethodsData was available from a sample of 6.5 year‐old twins, consisting of 369 mothers and 663 children and 255 fathers and 458 children. Self‐reports were used to assess mothers’ and fathers’ warmth. Child prosociality was assessed with the other‐parent report and experimental assessments.ResultsMothers’ warmth was not affected by their BDNF genotype, neither as a main effect nor in an interaction with child prosociality. Fathers with the Met allele scored higher on warmth. Additionally, there was a significant interaction between fathers’ BDNF genotype and child prosociality. For fathers with the Met allele there was a positive association between warmth and child prosociality. Conversely, for fathers with the Val/Val genotype there was no association between warmth and child prosociality. Results were repeated longitudinally in a subsample with data on age 8–9 years. A direct within family analysis showed that fathers with the Met allele were more likely than Val/Val carriers to exhibit differential parenting toward twins who differed in their prosocial behavior. The same pattern of findings was found with mother‐rated and experimentally assessed prosociality.ConclusionsThese results shed light on the genetic and environmental underpinnings of paternal behavior and differential parenting.

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Section: Discussionmentioning

confidence: 99%

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

Avinun

Knafo‐Noam

2017

Brain and Behavior

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“…Moreover, hippocampal slices from BDNF heterozygous mice displayed a significant decline of CAF LTP compared with WT. Previous experimental findings indicate that BDNF may be released at both pre‐ and postsynaptic levels (Lessmann & Brigadski 2009; Matsuda et al 2009; Edelmann et al 2014) and it is known that BDNF can significantly affect PPF (Kang & Schuman 1995). In our experiments, caffeine perfusion induced a significant change in PPF response suggesting an enhancement of the neurotransmitter release.…”

Section: Discussionmentioning

confidence: 99%

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

et al. 2016

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Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal and mood. These effects imply changes at circuital and synaptic level, but the mechanism by which caffeine modifies synaptic plasticity remains elusive. Here we report that caffeine, at concentrations representing moderate to high levels of consumption in humans, induces an NMDA receptor‐independent form of LTP (CAFLTP) in the CA1 region of the hippocampus by promoting calcium‐dependent secretion of BDNF, which subsequently activates TrkB‐mediated signaling required for the expression of CAFLTP. Our data include the novel observation that insulin receptor substrate 2 (IRS2) is phosphorylated during induction of CAFLTP, a process that requires cytosolic free Ca2+. Consistent with the involvement of IRS2 signals in caffeine‐mediated synaptic plasticity, phosphorylation of Akt (Ser473) in response to LTP induction is defective in Irs2−/− mice, demonstrating that these plasticity changes are associated with downstream targets of the phosphoinositide 3‐kinase (PI3K) pathway. These findings indicate that TrkB‐IRS2 signals are essential for activation of PI3K during the induction of LTP by caffeine.

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“…The most conspicuous mechanism might be the release of dense-core vesicles, such as shown to be involved in the release of various peptides, such as for example, BDNF release from neurons (e.g. [58]). This type of release, however, generally requires depolarization-induced intracellular Ca 2þ transients, which are difficult to conceive for long-lasting T3 actions, for these are most likely mediated by nuclear receptors (e.g.…”

Section: (B) Mechanisms Of Protein Secretion From Glial Cellsmentioning

confidence: 99%

Regulation of neuronal excitability by release of proteins from glial cells

Igelhorst

Niederkinkhaus

Karus

et al. 2015

Phil. Trans. R. Soc. B

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Effects of glial cells on electrical isolation and shaping of synaptic transmission between neurons have been extensively studied. Here we present evidence that the release of proteins from astrocytes as well as microglia may regulate voltage-activated Na þ currents in neurons, thereby increasing excitability and speed of transmission in neurons kept at distance from each other by specialized glial cells. As a first example, we show that basic fibroblast growth factor and neurotrophin-3, which are released from astrocytes by exposure to thyroid hormone, influence each other to enhance Na þ current density in cultured hippocampal neurons. As a second example, we show that the presence of microglia in hippocampal cultures can upregulate Na þ current density. The effect can be boosted by lipopolysaccharides, bacterial membrane-derived stimulators of microglial activation. Comparable effects are induced by the exposure of neuron-enriched hippocampal cultures to tumour necrosis factor-a, which is released from stimulated microglia. Taken together, our findings suggest that release of proteins from various types of glial cells can alter neuronal excitability over a time course of several days. This explains changes in neuronal excitability occurring in states of thyroid hormone imbalance and possibly also in seizures triggered by infectious diseases.

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Pre- and postsynaptic twists in BDNF secretion and action in synaptic plasticity

Cited by 216 publications

References 242 publications

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

Regulation of neuronal excitability by release of proteins from glial cells

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