BDNF mechanisms in late LTP formation: A synthesis and breakdown

Panja, Debabrata; Bramham, Clive R.

doi:10.1016/j.neuropharm.2013.06.024

Cited by 291 publications

(235 citation statements)

References 178 publications

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“…To determine how dendritic BDNF translation is regulated, we considered the main postsynaptic pathways activated by glutamate (Bramham and Wells, 2007;Panja and Bramham, 2014). The signaling cascades involved were dissected out by analyzing five major players of mRNA circularization and translation.…”

Section: Discussionmentioning

confidence: 99%

Signaling pathways controlling activity-dependent local translation of BDNF and their localization in dendritic arbors

Baj

Pinhero

Vaghi

et al. 2016

Journal of Cell Science

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Brain-derived neurotrophic factor (BDNF) is encoded by multiple mRNA variants whose differential subcellular distribution constitutes a 'spatial code' for local translation of BDNF and selective morphological remodeling of dendrites. Here, we investigated where BDNF translation takes place and what are the signaling pathways involved. Cultured hippocampal neurons treated with KCl showed increased BDNF in the soma, proximal and distal dendrites, even in quaternary branches. This activity-dependent increase of BDNF was abolished by cycloheximide, suggesting local translation, and required activation of glutamate and Trk receptors. Our data showed that BDNF translation was regulated by multiple signaling cascades including RAS-Erk and mTOR pathways, and CaMKII-CPEB1, Aurora-A-CPEB1 and Src-ZBP1 pathways. Aurora-A, CPEB1, ZBP1 (also known as IGF2BP1), eiF4E, S6 (also known as rpS6) were present throughout the dendritic arbor. Neuronal activity increased the levels of Aurora-A, CPEB1 and ZBP1 in distal dendrites whereas those of eiF4E and S6 were unaffected. BDNF-6, the main dendritic BDNF transcript, was translated in the same subcellular domains and in response to the same pathways as total BDNF. In conclusion, we identified the signaling cascades controlling BDNF translation and we describe how the translational machinery localization is modulated in response to electrical activity.

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Section: Discussionmentioning

confidence: 99%

Signaling pathways controlling activity-dependent local translation of BDNF and their localization in dendritic arbors

Baj

Pinhero

Vaghi

et al. 2016

Journal of Cell Science

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“…Therefore, understanding the involvement of the hippocampus in ORM reconsolidation is necessary to develop new therapies to prevent the pervasive recollection of distressing declarative memories and treat its consequences. Brain-Derived Neurotrophic Factor (BDNF) is a member of the neurotrophin family of growth factors essential for synapse formation and maintenance (Cowansage, LeDoux, & Monfils, 2010;Panja & Bramham, 2014). In the rat hippocampus, BDNF mediates spatial and recognition memory formation (Francis et al, 2012;Furini et al, 2010;Harvey et al, 2008;Petzold, Psotta, Brigadski, Endres, & Lessmann, 2015;Silhol, Arancibia, Maurice, & Tapia-Arancibia, 2007) and is sufficient for reconsolidation of fear extinction .…”

Section: Introductionmentioning

confidence: 99%

BDNF controls object recognition memory reconsolidation

Radiske

Rossato

Gonzalez

et al. 2017

Neurobiology of Learning and Memory

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a-amanitinMuscimol Novelty Retrieval a b s t r a c t Reconsolidation restabilizes memory after reactivation. Previously, we reported that the hippocampus is engaged in object recognition memory reconsolidation to allow incorporation of new information into the original engram. Here we show that BDNF is sufficient for this process, and that blockade of BDNF function in dorsal CA 1 impairs updating of the reactivated recognition memory trace.

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“…Brain-derived neurotrophic factor (BDNF) is a key regulator of protein-synthesis-dependent synaptic plasticity and memory formation in the mammalian brain (Bekinschtein et al, 2014;Minichiello, 2009;Panja and Bramham, 2014;Park and Poo, 2013).…”

Section: Introductionmentioning

confidence: 99%

Two-Stage Translational Control of Dentate Gyrus LTP Consolidation Is Mediated by Sustained BDNF-TrkB Signaling to MNK

et al. 2014

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BDNF signaling contributes to protein-synthesis-dependent synaptic plasticity, but the dynamics of TrkB signaling and mechanisms of translation have not been defined. Here, we show that long-term potentiation (LTP) consolidation in the dentate gyrus of live rodents requires sustained (hours) BDNF-TrkB signaling. Surprisingly, this sustained activation maintains an otherwise labile signaling pathway from TrkB to MAP-kinase-interacting kinase (MNK). MNK activity promotes eIF4F translation initiation complex formation and protein synthesis in mechanistically distinct early and late stages. In early-stage translation, MNK triggers release of the CYFIP1/FMRP repressor complex from the 5'-mRNA cap. In late-stage translation, MNK regulates the canonical translational repressor 4E-BP2 in a synapse-compartment-specific manner. This late stage is coupled to MNK-dependent enhanced dendritic mRNA translation. We conclude that LTP consolidation in the dentate gyrus is mediated by sustained BDNF signaling to MNK and MNK-dependent regulation of translation in two functionally and mechanistically distinct stages.

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BDNF mechanisms in late LTP formation: A synthesis and breakdown

Cited by 291 publications

References 178 publications

Signaling pathways controlling activity-dependent local translation of BDNF and their localization in dendritic arbors

Signaling pathways controlling activity-dependent local translation of BDNF and their localization in dendritic arbors

BDNF controls object recognition memory reconsolidation

Two-Stage Translational Control of Dentate Gyrus LTP Consolidation Is Mediated by Sustained BDNF-TrkB Signaling to MNK

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