scholarly journals Synaptic maturation of theXenopusretinotectal system: Effects of brain-derived neurotrophic factor on synapse ultrastructure

2010 ◽  
Vol 518 (7) ◽  
pp. 972-989 ◽  
Author(s):  
Angeliki Maria Nikolakopoulou ◽  
Margarita M. Meynard ◽  
Sonya Marshak ◽  
Susana Cohen-Cory
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Synapse Ultrastructure ◽  
Synaptic Maturation

scholarly journals Neuroligin-1 mediates presynaptic maturation through brain-derived neurotrophic factor signaling

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Andonia Petkova-Tuffy ◽  
Nina Gödecke ◽  
Julio Viotti ◽  
Martin Korte ◽  
Thomas Dresbach
Keyword(s):  
Cell Adhesion ◽  
Synaptic Vesicle ◽  
Neurotrophic Factor ◽  
Neurodevelopmental Disorders ◽  
Active Zone ◽  
Brain Derived Neurotrophic Factor ◽  
Synaptic Vesicle Recycling ◽  
Vesicle Recycling ◽  
Synapse Maturation ◽  
Synaptic Maturation

Abstract Background Maturation is a process that allows synapses to acquire full functionality, optimizing their activity to diverse neural circuits, and defects in synaptic maturation may contribute to neurodevelopmental disorders. Neuroligin-1 (NL1) is a postsynaptic cell adhesion molecule essential for synapse maturation, a role typically attributed to binding to pre-synaptic ligands, the neurexins. However, the pathways underlying the action of NL1 in synaptic maturation are incompletely understood, and some of its previously observed effects seem reminiscent of those described for the neurotrophin brain-derived neurotrophic factor (BDNF). Here, we show that maturational increases in active zone stability and synaptic vesicle recycling rely on the joint action of NL1 and brain-derived neurotrophic factor (BDNF). Results Applying BDNF to hippocampal neurons in primary cultures or organotypical slice cultures mimicked the effects of overexpressing NL1 on both structural and functional maturation. Overexpressing a NL1 mutant deficient in neurexin binding still induced presynaptic maturation. Like NL1, BDNF increased synaptic vesicle recycling and the augmentation of transmitter release by phorbol esters, both hallmarks of presynaptic maturation. Mimicking the effects of NL1, BDNF also increased the half-life of the active zone marker bassoon at synapses, reflecting increased active zone stability. Overexpressing NL1 increased the expression and synaptic accumulation of BDNF. Inhibiting BDNF signaling pharmacologically or genetically prevented the effects of NL1 on presynaptic maturation. Applying BDNF to NL1-knockout mouse cultures rescued defective presynaptic maturation, indicating that BDNF acts downstream of NL1 and can restore presynaptic maturation at late stages of network development. Conclusions Our data introduce BDNF as a novel and essential component in a transsynaptic pathway linking NL1-mediated cell adhesion, neurotrophin action, and presynaptic maturation. Our findings connect synaptic cell adhesion and neurotrophin signaling and may provide a therapeutic approach to neurodevelopmental disorders by targeting synapse maturation.

scholarly journals Glucocorticoid Prevents Brain-Derived Neurotrophic Factor-Mediated Maturation of Synaptic Function in Developing Hippocampal Neurons through Reduction in the Activity of Mitogen-Activated Protein Kinase

2008 ◽  
Vol 22 (3) ◽  
pp. 546-558 ◽  
Author(s):  
Emi Kumamaru ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Yuki Yagasaki ◽  
Aiko Izumi ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Neurotrophic Factor ◽  
Intracellular Signaling ◽  
Hippocampal Neurons ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Synaptic Function ◽  
Synaptic Proteins ◽  
Mature Stage ◽  
Synaptic Maturation

Abstract An increased level of glucocorticoid may be related to the pathophysiology of depressive disorder. The involvement of brain-derived neurotrophic factor (BDNF) in the antidepressive effect has also been suggested; however, the possible influence of glucocorticoid on the action of BDNF in the developing central nervous system has not been elucidated. In this study, we investigated the effect of glucocorticoid (dexamethasone, DEX) on synaptic maturation and function enhanced by BDNF in early developing hippocampal neurons. In the immature stage, BDNF increased the outgrowth of dendrites and the expression of synaptic proteins including glutamate receptors and presynaptic proteins. Pretreatment with DEX significantly inhibited the BDNF-dependent up-regulation of both dendritic outgrowth and synaptic proteins. In the more mature stage, the BDNF-reinforced postsynaptic Ca2+ influx was decreased by DEX. BDNF-enhanced presynaptic glutamate release was also suppressed. RU486, a glucocorticoid receptor antagonist, canceled the DEX-dependent blocking effect on the action of BDNF. After down-regulation of glucocorticoid receptor by small interfering RNA application, no inhibitory effect of DEX on the BDNF-increased synaptic proteins was observed. Interestingly, the BDNF-activated MAPK/ERK pathway, which is an essential intracellular signaling pathway for the BDNF-increased synaptic proteins, was reduced by DEX. These results suggest that BDNF-mediated synaptic maturation is disturbed after neurons are exposed to high-level glucocorticoid in their development stage.

Brain Derived Neurotrophic Factor Gene Polymorphism Associated With Language Acquisition

2007 ◽  
Author(s):  
Scott H. Fraundorf ◽  
Brad E. Sheese ◽  
Lauren K. White ◽  
Mary K. Rothbart ◽  
Michael I. Posner
Keyword(s):  
Language Acquisition ◽  
Gene Polymorphism ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Factor Gene
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