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MAP Kinase Translocates into the Nucleus of the Presynaptic Cell and Is Required for Long-Term Facilitation in Aplysia
Open accessAbstract
Long-term facilitation of the sensory to motor synapse in Aplysia requires gene expression. While some transcription factors involved in long-term facilitation are phosphorylated by PKA, others lack PKA sites but contain MAP Kinase (MAPK) phosphorylation sites. We now show that MAPK translocates into the nucleus of the presynaptic but not the postsynaptic cell during 5-HT-induced long-term facilitation. The presynaptic nuclear translocation of MAPK is also triggered by elevations in intracellular cAMP. Injection of anti-MAPK antibodies or of MAPK Kinase inhibitors into the presynaptic cell blocks long-term facilitation, without affecting basal synaptic transmission or short-term facilitation. Thus, MAPK appears to be specifically recruited and necessary for the long-term form of facilitation. This mechanism for long-term plasticity may be quite general: cAMP also activated MAPK in mouse hippocampal neurons, suggesting that MAPK may play a role in hippocampal long-term potentiation.
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“Two biochemical cascades required for LTF are those that mediate activation of protein kinase A (PKA)12–15 and the MAP kinase isoform termed extracellular signal-regulated kinase (ERK)16–18.”
From Computational design of enhanced learning protocols (2012) · cites this paper as [16]
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Metadata
- Authors
- Martin, K. C., Michael, D., Rose, J. C., Barad, M., Casadio, A., Zhu, H., & Kandel, E. R.
- Affiliations
- Howard Hughes Medical Institute (US)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Kandel, Eric R
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1997-06
- Volume
- 18
- Issue
- 6
- Pages
- 899-912
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2066592391
- Cited by
- 545
- References
- 68
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 8 · 2023: 5 · 2022: 9 · 2021: 9 · 2020: 9 · 2019: 11 · 2018: 13 · 2017: 14 · 2016: 13 · 2015: 14 · 2014: 16 · 2013: 16 · 2012: 14
- FWCI
- 16.93
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuron (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- mitogen-activated protein kinase, nuclear translocation, long-term facilitation, Aplysia, serotonin, cyclic AMP, synaptic plasticity, gene expression, hippocampal long-term potentiation
- MeSH terms
- Cyclic AMP, Amino Acid Sequence, Animals, Aplysia, Cell Compartmentation, Cell Nucleus, Cells, Cultured, Enzyme Inhibitors, Flavonoids, Colforsin, Hippocampus, Molecular Sequence Data, Synaptic Transmission, Neuronal Plasticity, Neurons, Afferent, Peptides, Protein-Tyrosine Kinases, Serotonin, Synapses, Protein Serine-Threonine Kinases, Presynaptic Terminals, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Mitogen-Activated Protein Kinase Kinases, MAP Kinase Kinase 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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