Stowers Institute for Medical Research, Kansas City, United States
Yunming Wu
Stowers Institute for Medical Research, Kansas City, United States
Limei Ma
Stowers Institute for Medical Research, Kansas City, United States
Wenjing Xu
Stowers Institute for Medical Research, Kansas City, United States
Max Hills Jr
Stowers Institute for Medical Research, Kansas City, United States
Vivekanandan Ramalingam
Stowers Institute for Medical Research, Kansas City, United States; Interdisciplinary Graduate Program in Biomedical Sciences, University of Kansas Medical Center, Kansas City, United States
Stowers Institute for Medical Research, Kansas City, United States; Interdisciplinary Graduate Program in Biomedical Sciences, University of Kansas Medical Center, Kansas City, United States; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, United States
Animals possess an inborn ability to recognize certain odors to avoid predators, seek food, and find mates. Innate odor preference is thought to be genetically hardwired. Here we report that acquisition of innate odor recognition requires spontaneous neural activity and is influenced by sensory experience during early postnatal development. Genetic silencing of mouse olfactory sensory neurons during the critical period has little impact on odor sensitivity, discrimination, and recognition later in life. However, it abolishes innate odor preference and alters the patterns of activation in brain centers. Exposure to innately recognized odors during the critical period abolishes the associated valence in adulthood in an odor-specific manner. The changes are associated with broadened projection of olfactory sensory neurons and expression of axon guidance molecules. Thus, a delicate balance of neural activity is needed during the critical period in establishing innate odor preference and convergent axon input is required to encode innate odor valence.