Cleavage of proBDNF by tPA/Plasmin Is Essential for Long-Term Hippocampal Plasticity
@article{Pang2004CleavageOP,
title={Cleavage of proBDNF by tPA/Plasmin Is Essential for Long-Term Hippocampal Plasticity},
author={Petti T. Pang and Henry K Teng and Eugene Zaitsev and Newton T Woo and Kazuko Sakata and Shushuang Zhen and Kenneth K. Teng and Wing-Ho Yung and Barbara L. Hempstead and Bai Lu},
journal={Science},
year={2004},
volume={306},
pages={487 - 491}
}Long-term memory is thought to be mediated by protein synthesis–dependent, late-phase long-term potentiation (L-LTP). Two secretory proteins, tissue plasminogen activator (tPA) and brain-derived neurotrophic factor (BDNF), have been implicated in this process, but their relationship is unclear. Here we report that tPA, by activating the extracellular protease plasmin, converts the precursor proBDNF to the mature BDNF (mBDNF), and that such conversion is critical for L-LTP expression in mouse…
1,038 Citations
Matrix Metalloproteinase-9 Is Required for Hippocampal Late-Phase Long-Term Potentiation and Memory
- Biology, PsychologyThe Journal of Neuroscience
- 2006
A novel role for MMP-9 is demonstrated in hippocampal synaptic physiology, plasticity, and memory and integrin function-blocking reagents prevent an M MP-9-mediated potentiation of synaptic signal strength.
Regulation of late-phase LTP and long-term memory in normal and aging hippocampus: role of secreted proteins tPA and BDNF
- BiologyAgeing Research Reviews
- 2004
BDNF: A key regulator for protein synthesis-dependent LTP and long-term memory?
- BiologyNeurobiology of Learning and Memory
- 2008
Extracellular proteolysis of reelin by tissue plasminogen activator following synaptic potentiation
- BiologyNeuroscience
- 2014
Proteolysis of proBDNF Is a Key Regulator in the Formation of Memory
- Biology, PsychologyPloS one
- 2008
The differential requirement for the processing of proBDNF by tPA in distinct memory processes suggest that the molecular events actively engaged to support the storage and/or the successful retrieval of memory depends on the integration of ongoing experience with past learning.
Tissue plasminogen activator in the amygdala: a new role for an old protease.
- Biology, PsychologyJournal of physiology and pharmacology : an official journal of the Polish Physiological Society
- 2008
tPA-mediated facilitation of experience-induced plasticity in the limbic system is mediated by a complex mechanism that may involve direct or indirect interactions of tPA with NMDA receptor, its binding to the LRP receptor or activation of brain-derived growth factor.
BDNF Facilitates L-LTP Maintenance in the Absence of Protein Synthesis through PKMζ
- BiologyPloS one
- 2011
It is suggested that brain-derived neurotrophic factor sustains L-LTP through PKMζ in a protein synthesis-independent manner, revealing an unexpected link between BDNF and PKM ζ.
A tropomyosin-related kinase B ligand is required for ERK activation, long-term synaptic facilitation, and long-term memory in Aplysia
- BiologyProceedings of the National Academy of Sciences
- 2006
Results show that a secreted growth factor, acting through a TrkB signaling cascade, is critical for the induction of long-lasting plasticity and memory formation in Aplysia.
Neuropsin—A possible modulator of synaptic plasticity
- Biology, PsychologyJournal of Chemical Neuroanatomy
- 2011
GluN2D Subunit-Containing NMDA Receptors Control Tissue Plasminogen Activator-Mediated Spatial Memory
- Biology, PsychologyThe Journal of Neuroscience
- 2012
The data provide the first evidence that tPA influences spatial memory through its preferential interaction with GluN2D subunit-containing NMDARs.
References
SHOWING 1-10 OF 30 REFERENCES
A different form of long-lasting potentiation revealed in tissue plasminogen activator mutant mice
- BiologyThe Journal of neuroscience : the official journal of the Society for Neuroscience
- 1996
Analysis of long-lasting LTP in CA1 hippocampal slices of mice homozygous for disrupted t-PA genes provides evidence that these mice are devoid of conventional homosynaptic L-LTP at the Schaffer collateral-CA1 pyramidal cell synapse.
Tissue Plasminogen Activator Contributes to the Late Phase of LTP and to Synaptic Growth in the Hippocampal Mossy Fiber Pathway
- BiologyNeuron
- 1998
Tissue-plasminogen activator is induced as an immediate–early gene during seizure, kindling and long-term potentiation
- BiologyNature
- 1993
Differential screening is used to identify five immediate–early genes induced by neuronal activity that play a role in the structural changes that accompany activity-dependent plasticity and tissue-plasminogen activator (tPA) is one of these.
Laminin Degradation by Plasmin Regulates Long-Term Potentiation
- BiologyThe Journal of Neuroscience
- 2000
The results suggest that the laminin-mediated cell–ECM interaction may be necessary for the maintenance of LTP and that the PA–plasmin system regulates synaptic plasticity.
A role for BDNF in the late-phase of hippocampal long-term potentiation
- BiologyNeuropharmacology
- 1998
Proteolysis of cell adhesion molecules by serine proteases: a role in long term potentiation?
- BiologyBrain Research
- 1998
Genetic Demonstration of a Role for PKA in the Late Phase of LTP and in Hippocampus-Based Long-Term Memory
- Biology, PsychologyCell
- 1997
Some Forms of cAMP-Mediated Long-Lasting Potentiation Are Associated with Release of BDNF and Nuclear Translocation of Phospho-MAP Kinase
- BiologyNeuron
- 2001
Tissue plasminogen activator controls multiple forms of synaptic plasticity and memory
- Biology, PsychologyThe European journal of neuroscience
- 2000
Electrophysiological recordings obtained from hippocampal slices in the CA1 area showed that mainly the late phase of long‐term potentiation was reduced in t‐PA‐KO mice, suggesting an altered striatal function.
Long-lasting neurotrophin-induced enhancement of synaptic transmission in the adult hippocampus
- BiologyScience
- 1995
Long-term potentiation could still be elicited in slices previously potentiated by exposure to the neurotrophic factors, which implies that these two forms of plasticity may use at least partially independent cellular mechanisms.