This is a proposed model in which BDNF signaling supports protein synthesis-dependent late-phase LTP through synaptic consolidation mechanisms. The abstract links it to Arc transcription, dendritic mRNA trafficking, and local translation.
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synaptic consolidation hypothesis
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BDNF activates distinct mechanisms to regulate the induction, early maintenance, and late maintenance phases of LTP.
BDNF activates distinct mechanisms to regulate the induction, early maintenance, and late maintenance phases of LTP.
Recent experiments summarized in the review suggest that BDNF activates synaptic consolidation through transcription and rapid dendritic trafficking of Arc mRNA.
Recent experiments suggest that BDNF activates synaptic consolidation through transcription and rapid dendritic trafficking of mRNA encoded by the immediate early gene, Arc.
The review emphasizes BDNF as a trigger for protein synthesis-dependent late-phase LTP, referred to as synaptic consolidation.
Particular attention is given to the role of BDNF as a trigger for protein synthesis-dependent late phase LTP--a process referred to as synaptic consolidation.
The specific contribution of BDNF to LTP depends on the stimulus pattern used to induce LTP, which affects the duration and possibly the subcellular site of BDNF release.
The specific contribution of BDNF depends on the stimulus pattern used to induce LTP, which impacts the duration and perhaps the subcellular site of BDNF release.
A proposed model is that BDNF signaling at glutamate synapses drives translation of newly transported Arc mRNA and locally stored alphaCaMKII mRNA in dendrites, tags synapses for mRNA capture, and that Arc translation defines a critical window for synaptic consolidation.
A model is proposed in which BDNF signaling at glutamate synapses drives the translation of newly transported (Arc) and locally stored (i.e., alphaCaMKII) mRNA in dendrites. In this model BDNF tags synapses for mRNA capture, while Arc translation defines a critical window for synaptic consolidation.