Commentary: Anxiety- and Depression-like States Lead to Pronounced Olfactory Deficits and Impaired Adult Neurogenesis in Mice.

Jeremy C Borniger,Yasmine M Cissé,Monica M Gaudier-Diaz,William H Walker Ii

doi:10.3389/fnbeh.2016.00130

Jeremy C Borniger, Yasmine M Cissé + Show 2 more

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https://doi.org/10.3389/fnbeh.2016.00130

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Abstract

Commentary: Anxiety- and Depression-like States Lead to Pronounced Olfactory Deficits and Impaired Adult Neurogenesis in Mice.

Highlights

Neuroscience Graduate Program and Behavioral Neuroendocrinology Group, Department of Neuroscience, The Ohio State University – Wexner Medical Center, Columbus, OH, USA
The hippocampus has become central in affective disorder research because blocking hippocampal neurogenesis eliminates some beneficial effects of monoaminergic antidepressants (Surget et al, 2008), whereas increasing neurogenesis reduces glucocorticoid-induced anxiety- and depressive-like responses (Hill et al, 2015)
Subventricular zone (SVZ) neuroblasts migrate to the olfactory bulb (OB) along the rostral migratory stream (RMS)

Summary

Introduction

A commentary on Anxiety- and Depression-like States Lead to Pronounced Olfactory Deficits and Impaired Adult Neurogenesis in Mice by Siopi, E., Denizet, M., Gabellec, M. The hippocampus has become central in affective disorder research because blocking hippocampal neurogenesis eliminates some beneficial effects of monoaminergic antidepressants (Surget et al, 2008), whereas increasing neurogenesis reduces glucocorticoid-induced anxiety- and depressive-like responses (Hill et al, 2015). Olfactory neurogenesis occurs in humans (Curtis et al, 2007); patients with major depression display impaired olfactory function and sensitivity; it is unknown whether these changes are related to glucocorticoid dysregulation and reduced neurogenesis that often accompanies depressive disorders.

Results

Conclusion