Abstract
Long-term potentiation (LTP) and long-term depression (LTD) are the major forms of functional synaptic plasticity observed at CA1 synapses of the hippocampus. The balance between LTP and LTD or "metaplasticity" is controlled by G-protein coupled receptors (GPCRs) whose signal pathways target the N-methyl-D-asparate (NMDA) subtype of excitatory glutamate receptor. We discuss the protein kinase signal cascades stimulated by Galphaq and Galphas coupled GPCRs and describe how control of NMDAR activity shifts the threshold for the induction of LTP.
MeSH terms
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Animals
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Cyclic AMP-Dependent Protein Kinases / metabolism
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Hippocampus / cytology
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Hippocampus / metabolism
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Hippocampus / physiology*
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Humans
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Intercellular Signaling Peptides and Proteins / genetics
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Neuronal Plasticity* / genetics
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Neurons / metabolism
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Neurons / physiology
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Protein-Tyrosine Kinases / metabolism
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Receptors, G-Protein-Coupled / genetics
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Receptors, G-Protein-Coupled / physiology*
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Receptors, N-Methyl-D-Aspartate / genetics
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide / genetics
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Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide / physiology*
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Transcriptional Activation
Substances
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Intercellular Signaling Peptides and Proteins
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Receptors, G-Protein-Coupled
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Receptors, N-Methyl-D-Aspartate
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Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide
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Protein-Tyrosine Kinases
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Cyclic AMP-Dependent Protein Kinases