Abstract
The active zone protein RIM1alpha is required both for maintaining normal probability of neurotransmitter release and for long-term presynaptic potentiation at brain synapses. We now demonstrate that RIM1alpha(-/-) mice exhibit normal coordination and anxiety-related behaviors but display severely impaired learning and memory. Mice with a synaptotagmin 1 mutation, which selectively lowers release probability, and mice with Rab3A deletion, which selectively abolishes presynaptic long-term potentiation, do not exhibit this abnormality. Our data suggest that a decrease in release probability or a loss of presynaptic LTP alone is not sufficient to cause major behavioral alterations, but the combination of presynaptic abnormalities in RIM1alpha(-/-) mice severely alters learning and memory.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Behavior, Animal
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Blotting, Western / methods
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Brain / metabolism
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Calcium-Binding Proteins*
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Conditioning, Classical / physiology
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Fear / physiology
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GTP-Binding Proteins / physiology*
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In Situ Hybridization / methods
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Learning / physiology
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Maze Learning / physiology
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Membrane Glycoproteins / physiology
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Memory / physiology*
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Mice
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Mice, Knockout
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Motor Activity / genetics
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Nerve Tissue Proteins / physiology*
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Psychomotor Performance / physiology
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Reaction Time / genetics
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Space Perception / physiology
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Spatial Behavior / physiology
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Synaptotagmin I
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Synaptotagmins
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Time Factors
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rab3A GTP-Binding Protein / physiology
Substances
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Calcium-Binding Proteins
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Membrane Glycoproteins
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Nerve Tissue Proteins
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Rim protein, mammalian
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Rims1 protein, mouse
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Synaptotagmin I
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Syt1 protein, mouse
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Synaptotagmins
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GTP-Binding Proteins
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rab3A GTP-Binding Protein