Abstract
Although nerve growth factor (NGF) is a crucial factor in the activity-dependent development and plasticity of visual cortex, its role in synaptic efficacy changes is largely undefined. We demonstrate that the maintenance phase of long-term potentiation (LTP) is blocked by local application of exogenous NGF in rat visual cortex at an early stage of postnatal development. Long-term depression (LTD) and bidirectional plasticity are unaffected. At later postnatal ages, blockade of either endogenous NGF by immunoadhesin (TrkA-IgG) or TrkA receptors by monoclonal antibody rescues LTP. Muscarinic receptor activation/inhibition suggests that LTP dependence on NGF is mediated by the cholinergic system. These results indicate that NGF regulates synaptic strength in well-characterized cortical circuitries.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Antibody Specificity
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Atropine / pharmacology
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / physiology
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Immunoglobulin G / pharmacology
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Lysine / analogs & derivatives
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Lysine / pharmacokinetics
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Muscarinic Antagonists / pharmacology
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Nerve Growth Factor / immunology
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Nerve Growth Factor / metabolism*
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Nerve Growth Factor / pharmacology
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology
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Neurons / chemistry
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Neurons / cytology
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Neurons / metabolism
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PC12 Cells
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Rats
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Rats, Wistar
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Receptor, trkA / antagonists & inhibitors*
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Receptor, trkA / immunology
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Receptor, trkA / metabolism
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Receptors, Cholinergic / physiology*
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Visual Cortex / cytology
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Visual Cortex / growth & development
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Visual Cortex / metabolism*
Substances
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Antibodies, Monoclonal
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Immunoglobulin G
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Muscarinic Antagonists
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Receptors, Cholinergic
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Atropine
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Nerve Growth Factor
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Receptor, trkA
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biocytin
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Lysine