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The Journal of Neuroscience, August 29, 2007, 27(35):9427-9438; doi:10.1523/JNEUROSCI.0664-07.2007

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Development/Plasticity/Repair
Experience-Dependent Modification of Primary Sensory Synapses in the Mammalian Olfactory Bulb

William J. Tyler, Gabor C. Petzold, Sumon K. Pal, and Venkatesh N. Murthy

Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138

Correspondence should be addressed to Dr. William J. Tyler at his present address: School of Life Sciences, Arizona State University, Box 874501, Tempe, AZ 85287-4501. Email: wtyler{at}asu.edu

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.

Key words: olfactory bulb; glomerulus; odor deprivation; sensory scaling; olfactory sensory axon; compensatory plasticity

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Received Feb. 14, 2007; revised June 19, 2007; accepted July 16, 2007.

Correspondence should be addressed to Dr. William J. Tyler at his present address: School of Life Sciences, Arizona State University, Box 874501, Tempe, AZ 85287-4501. Email: wtyler{at}asu.edu

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