Persistent activation of the zeta isoform of protein kinase C in the maintenance of long-term potentiation
Todd Charlton Sacktor,Pavel Osten,Helen Valsamis,Xiaolan Jiang,Meghna U. Naik,Elizabeth Sublette +5 more
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TLDR
The transition from translocation of PKC to formation of PKM may help to explain the molecular mechanisms of induction and maintenance of long-term potentiation.Abstract:
Long-term potentiation in the CA1 region of the hippocampus, a model for memory formation in the brain, is divided into two phases. A transient process (induction) is initiated, which then generates a persistent mechanism (maintenance) for enhancing synaptic strength. Protein kinase C (PKC), a gene family of multiple isozymes, may play a role in both induction and maintenance. In region CA1 from rat hippocampal slices, most of the isozymes of PKC translocated to the particulate fraction 15 sec after a tetanus. The increase of PKC in the particulate fraction did not persist into the maintenance phase of long-term potentiation. In contrast, a constitutively active kinase, PKM, a form specific to a single isozyme (zeta), increased in the cytosol during the maintenance phase. The transition from translocation of PKC to formation of PKM may help to explain the molecular mechanisms of induction and maintenance of long-term potentiation.read more
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GAP-43: an intrinsic determinant of neuronal development and plasticity.
TL;DR: In transgenic mice, overexpression of GAP-43 leads to the spontaneous formation of new synapses and enhanced sprouting after injury, and the protein might play an important role in mediating experience-dependent plasticity.
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Storage of Spatial Information by the Maintenance Mechanism of LTP
Eva Pastalkova,Peter A. Serrano,Deana Pinkhasova,Emma Jane Claire Wallace,André A. Fenton,Todd Charlton Sacktor +5 more
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Yong-hui Jiang,Dawna L. Armstrong,Urs Albrecht,Coleen M. Atkins,Jeffrey L. Noebels,Gregor Eichele,J. D. Sweatt,Arthur L. Beaudet,Arthur L. Beaudet +8 more
TL;DR: The cytoplasmic abundance of p53 was increased in postmitotic neurons in m-/p+ mice and in AS, providing a potential biochemical basis for the phenotype through failure to ubiquitinate and degrade various effectors.
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Postsynaptic protein phosphorylation and LTP.
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OLFACTORY MEMORY FORMATION IN DROSOPHILA: From Molecular to Systems Neuroscience
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References
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Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice
Alcino J. Silva,Alcino J. Silva,Charles F. Stevens,Charles F. Stevens,Susumu Tonegawa,Susumu Tonegawa,Yanyan Wang,Yanyan Wang +7 more
TL;DR: W Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact and are therefore a suitable model for studying the relation between LTP and learning processes.
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Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP.
TL;DR: Both postsynaptic PKC and CaMKII are required for the induction of LTP and a presynaptic protein kinase appears to be necessary for the expression of L TP, and both post synapses and protein kinases are sensitive to externally applied H-7.
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Intracellular injections of EGTA block induction of hippocampal long-term potentiation
TL;DR: It is reported that intracellular injections of the calcium chelator EGTA block the development of LTP and this results strongly suggest that LTP is caused by a modification of the postsynaptic neurone and that its induction depends on the level of free calcium.
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An essential role for postsynaptic calmodulin and protein kinase activity in long-term potentiation
Robert C. Malenka,Julie A. Kauer,David J. Perkel,Michael D. Mauk,Paul T. Kelly,Roger A. Nicoll,M. Neal Waxham +6 more
TL;DR: It is found that intracellular injection into CA1 pyramidal cells of the protein kinase inhibitor H-7, or of the calmodulin antagonist calmidazolium, blocks LTP, and LTP is blocked by the injection of synthetic peptides that are potentCalmodulin antagonists and inhibit CaM-KII auto- and substrate phosphorylation.