Abstract
A question of critical importance confronting neuroscientists today is how biochemical signals initiated at a synapse are conveyed to the nucleus. This problem is particularly relevant to the generation of the late phases of long-term potentiation (LTP). Here we provide evidence that some signaling pathways previously associated with late-LTP can be activated in hippocampal CA1 neurons without synaptic activity; somatic action potentials, induced by backfiring the cells, were found to be sufficient for phosphorylation of extracellular signal-regulated kinase-1/2 and cAMP response element-binding protein, as well as for induction of zif268. Furthermore, such antidromic stimulation was adequate to rescue "tagged" synapses (early-LTP) from decay. These results show that a synapse-to-nucleus signal is not necessary for late-phase LTP-associated signaling cascades in the regulation of gene expression.
MeSH terms
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Action Potentials* / drug effects
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Animals
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Cell Nucleus / drug effects
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Cell Nucleus / metabolism
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Cyclic AMP Response Element-Binding Protein / metabolism
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DNA-Binding Proteins / metabolism
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Early Growth Response Protein 1
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Gene Expression Regulation / drug effects
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Hippocampus / cytology
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Hippocampus / drug effects
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Hippocampus / metabolism*
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Immediate-Early Proteins*
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In Vitro Techniques
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Kynurenic Acid / pharmacology
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Long-Term Potentiation* / drug effects
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Mitogen-Activated Protein Kinases / metabolism
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Neurons / cytology
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Neurons / drug effects
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Neurons / metabolism*
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Nifedipine / pharmacology
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Phosphorylation / drug effects
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Rats
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Rats, Sprague-Dawley
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Signal Transduction / drug effects
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Synapses / drug effects
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Synapses / metabolism
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Transcription Factors / metabolism
Substances
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Cyclic AMP Response Element-Binding Protein
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DNA-Binding Proteins
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Early Growth Response Protein 1
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Egr1 protein, rat
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Immediate-Early Proteins
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Transcription Factors
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Mitogen-Activated Protein Kinases
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Kynurenic Acid
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Nifedipine