Abstract

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.

Highlights

  • Behavioral characteristics are often described as either acquired or innate

  • Spontaneous activity of the Olfactory sensory neurons (OSNs) is required for innate odor recognition

  • We found that there was no discernible difference in the amplitude and time course of odor-evoked responses between control and Kir2.1-off mice (Figure 1C)

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Summary

Introduction

While most environmental stimuli do not carry obvious ethological values, animals can develop characteristic responses through associative learning and assign valence to individual stimuli. Animals react innately to some stimuli with instinctive responses that are thought to be pre-programmed in the neural circuits. These stereotypic responses likely have evolved to deal with stimuli in the animal’s immediate environment that carry information about the inherent values of the signals. Innate behaviors are defined by stereotypical responses to the stimuli without prior experiences or associative learning, suggesting that neural circuits processing the inherent valence of stimuli are genetically hardwired to channel sensory information directly to the motor or endocrine output

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