Journal
CURRENT BIOLOGY
Volume 30, Issue 1, Pages 31-+Publisher
CELL PRESS
DOI: 10.1016/j.cub.2019.11.006
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Funding
- National Institute on Deafness and Other Communication Disorders [R01 DC006213, F31 DC017054]
- National Institute of Mental Health [T32 MH017168]
- National Institute of Health, United States
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Predicting danger from previously associated sensory stimuli is essential for survival. Contributions from altered peripheral sensory inputs are implicated in this process, but the underlying mechanisms remain elusive. Here, we use the mammalian olfactory system to investigate such mechanisms. Primary olfactory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli, where their synaptic release is subject to local and cortical influence and neuromodulation. Pairing optogenetic activation of a single glomerulus with foot shock in mice induces freezing to light stimulation alone during fear retrieval. This is accompanied by an increase in OSN release probability and a reduction in GABA(B) receptor expression in the conditioned glomerulus. Furthermore, freezing time is positively correlated with the release probability of OSNs in fear-conditioned mice. These results suggest that aversive learning increases peripheral olfactory inputs at the first synapse, which may contribute to the behavioral outcome.
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