| Autor: |
Glinka ME; Department of Neuroscience and the Howard Hughes Medical Institute, Columbia University, New York, NY 10032, USA., Samuels BA, Diodato A, Teillon J, Feng Mei D, Shykind BM, Hen R, Fleischmann A |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2012 May 09; Vol. 32 (19), pp. 6718-25. |
| DOI: |
10.1523/JNEUROSCI.4287-11.2012 |
| Abstrakt: |
Anxiety disorders are characterized by persistent fear in the absence of immediate threat and represent the most common psychiatric diseases, with an estimated 28% lifetime prevalence worldwide (Kessler et al., 2010). While symptoms of anxiety are typically evoked by sensory stimuli, it is unknown whether sensory deficits contribute to the development of anxiety disorders. Here we examine the effect of defined genetic mutations that compromise the function of the olfactory system on the development of anxiety-like behaviors in mice. We show that the functional inactivation of the main olfactory epithelium, but not the vomeronasal organ, causes elevated levels of anxiety. Anxiety-like behaviors are also observed in mice with a monoclonal nose, that are able to detect and discriminate odors but in which the patterns of odor-evoked neural activity are perturbed. In these mice, plasma corticosterone levels are elevated, suggesting that olfactory deficits can lead to chronic stress. These results demonstrate a central role for olfactory sensory cues in modulating anxiety in mice. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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