Abstract
Experience-dependent changes in neural circuits have traditionally been investigated several synapses downstream of sensory input. Whether experience can alter the strength of primary sensory synapses remains mostly unknown. To address this issue, we investigated the consequences of odor deprivation on synapses made by olfactory sensory axons in the olfactory bulb of rats. Odor deprivation triggered an increase in the probability of glutamate release from olfactory sensory neuron synapses. Deprivation also increased the amplitude of quantal synaptic currents mediated by AMPA- and NMDA-type glutamate receptors, as well as the abundance of these receptors in the glomerular region. Our results demonstrate that sensory experience is capable of modulating synaptic strength at the earliest stages of information transfer between the environment and an organism. Such compensatory experience-dependent changes may represent a mechanism of sensory gain control.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Animals, Newborn
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Bromodeoxyuridine / metabolism
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Caspase 3 / metabolism
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Cell Count / methods
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Electric Stimulation / methods
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Excitatory Amino Acid Agents / pharmacology
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / radiation effects
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Membrane Potentials / physiology
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Membrane Potentials / radiation effects
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N-Methylaspartate / metabolism
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Nerve Tissue Proteins / metabolism
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Neuronal Plasticity / physiology*
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Olfactory Bulb / cytology*
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Olfactory Receptor Neurons / cytology*
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Patch-Clamp Techniques / methods
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Rats
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Rats, Sprague-Dawley
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Sensory Deprivation / physiology
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Synapses / physiology*
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alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / metabolism
Substances
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Excitatory Amino Acid Agents
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Excitatory Amino Acid Antagonists
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Nerve Tissue Proteins
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N-Methylaspartate
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alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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Caspase 3
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Bromodeoxyuridine