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Journal ArticleDOI

Neurotrophin regulation of neural circuit development and function

Hyungju Park, +1 more
- 01 Jan 2013 - 
- Vol. 14, Iss: 1, pp 7-23
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TLDR
Some of the recent progress in understanding the cellular and molecular mechanisms underlying neurotrophin regulation of neural circuits are summarized in this Review.
Abstract
Brain-derived neurotrophic factor (BDNF)--a member of a small family of secreted proteins that includes nerve growth factor, neurotrophin 3 and neurotrophin 4--has emerged as a key regulator of neural circuit development and function. The expression, secretion and actions of BDNF are directly controlled by neural activity, and secreted BDNF is capable of mediating many activity-dependent processes in the mammalian brain, including neuronal differentiation and growth, synapse formation and plasticity, and higher cognitive functions. This Review summarizes some of the recent progress in understanding the cellular and molecular mechanisms underlying neurotrophin regulation of neural circuits. The focus of the article is on BDNF, as this is the most widely expressed and studied neurotrophin in the mammalian brain.

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Citations
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Rapid Modulation of Protein Expression in the Rat Hippocampus Following Deep Brain Stimulation of the Fornix.

TL;DR: Forniceal DBS triggers hippocampal activity and rapidly modulate the expression of neurotrophic factors and markers of synaptic plasticity known to play key roles in memory processing.
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Metalloproteinase inhibition prevents inhibitory synapse reorganization and seizure genesis.

TL;DR: Observations indicate that PNN degradation may be necessary for the development of seizures by facilitating interneuron plasticity and increased GABAergic activity.
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Structural basis for extracellular cis and trans RPTPσ signal competition in synaptogenesis

TL;DR: It is proposed that transient RPTPσ ectodomain emergence from the presynaptic proteoglycan layer allows capture by TrkC to form a trans-synaptic complex, the consequent reduction inRPTPσ flexibility potentiating interactions with additional ligands to orchestrate excitatory synapse formation.
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A role for the endocannabinoid system in exercise‐induced spatial memory enhancement in mice

TL;DR: The results suggest that, at least in part, the promnesic effect of the exercise is dependent of CB1 receptor activation and is mediated by BDNF, which can be mimic by inhibition of anandamide hydrolysis in sedentary animals.
References
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Journal ArticleDOI

The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function

TL;DR: A role is demonstrated for BDNF and its val/met polymorphism in human memory and hippocampal function and it is suggested val/ met exerts these effects by impacting intracellular trafficking and activity-dependent secretion of BDNF.
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The nerve growth factor 35 years later

TL;DR: The field of experimental embryology, which had been enthusiastically acclaimed in the mid-thirties, suffered from a sharp decrease in the enthusiasm that had inflamed the pioneers in this field, ever since R. G. Harrison delivered his celebrated lecture at the Royal Society in London in 1935.
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Synaptic Activity and the Construction of Cortical Circuits

TL;DR: The sequential combination of spontaneously generated and experience-dependent neural activity endows the brain with an ongoing ability to accommodate to dynamically changing inputs during development and throughout life.
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Neurotrophins and their receptors: a convergence point for many signalling pathways.

TL;DR: Recent findings that neurotrophins, in addition to promoting survival and differentiation, exert various effects through surprising interactions with other receptors and ion channels are reviewed.
Journal ArticleDOI

Physiology of the neurotrophins

TL;DR: Rapid actions of neurotrophin-3 on synaptic efficacy, as well as the regulation of their mRNAs by electrical activity, suggest that neurotrophins might play important roles in regulating neuronal connectivity in the developing and in the adult central nervous system.
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