Abstract
Dendritic spines at excitatory synapses undergo rapid, actin-dependent shape changes which may contribute to plasticity in brain circuits. Here we show that actin dynamics in spines are potently inhibited by activation of either AMPA or NMDA subtype glutamate receptors. Activation of either receptor type inhibited actin-based protrusive activity from the spine head. This blockade of motility caused spines to round up so that spine morphology became both more stable and more regular. Inhibition of spine motility by AMPA receptors was dependent on postsynaptic membrane depolarization and influx of Ca 2+ through voltage-activated channels. In combination with previous studies, our results suggest a two-step process in which spines initially formed in response to NMDA receptor activation are subsequently stabilized by AMPA receptors.
MeSH terms
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Actins / metabolism*
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Animals
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Calcium / metabolism
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Cell Movement / drug effects
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Cell Movement / physiology
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Cell Size / drug effects
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Cell Size / physiology*
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Cells, Cultured
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Dendrites / drug effects
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Dendrites / metabolism*
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Dendrites / ultrastructure
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Green Fluorescent Proteins
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / ultrastructure
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Luminescent Proteins / genetics
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Mice
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Mice, Transgenic
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology*
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Organ Culture Techniques
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Receptors, AMPA / drug effects
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Receptors, AMPA / metabolism
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Receptors, Glutamate / drug effects
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Receptors, Glutamate / metabolism*
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / metabolism
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Synapses / drug effects
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Synapses / metabolism*
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Synapses / ultrastructure
Substances
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Actins
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Luminescent Proteins
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Receptors, AMPA
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Receptors, Glutamate
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Receptors, N-Methyl-D-Aspartate
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Green Fluorescent Proteins
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Calcium