
A section of the olfactory epithelium from a mouse that had one nostril blocked, with a subtype of olfactory neurons shown in green and proliferating cells shown in magenta. Image credit: Hossain et al. (CC BY 4.0)
Wine tasters and perfumers are living proof that repeated exposure to specific scents can make humans more sensitive to them in the long-term. The sense of smell in humans and other mammals relies on millions of odor-sensing neurons, which detect scent molecules inhaled through the nose and send signals to the brain. There are many different ‘subtypes’ of these neurons, each of which detects specific odors.
The olfactory epithelium, a tissue lining the nasal cavity, produces odor-sensing neurons through a process called neurogenesis. It has long been assumed that this serves only to replace dead neurons and not to enable changes in the neuron population. This is because the subtype of each new neuron is thought to be random, so should be unaffected by exposure to odors. Yet, a more recent study in mice revealed that blocking one nostril reduces how frequently odor-sensing neurons of some subtypes are generated. However, these experiments did not reveal the type of stimuli that influence neurogenesis in the olfactory epithelium.
To investigate the possibility that these stimuli are specific odors, Hossain et al. exposed mice to odors emitted by male mice or musk odors, which are known to activate specific subtypes of odor-sensing neurons. Genetic and image-based analyses of the olfactory epithelium revealed that this exposure selectively accelerated the generation of neurons that respond to these odors. This suggests that neurogenesis does not just replace ‘lost’ cells but also allows the olfactory epithelium to adapt to scent exposure.
Hossain et al. hypothesize that this odor-specific neurogenesis could be one mechanism that allows mammals to ‘train’ their noses to be more sensitive to specific scents. In the future, these findings could help to develop treatments that restore the sense of smell in people who have lost sensory neurons.