The effect of temporary anosmia on olfactory bulb glomerular neuron activation

Neuroplasticity refers to changes in signaling and circuitry throughout the nervous system. The olfactory system is well known for its ability to induce neuroplasticity throughout the lifespan of the organism. Changes in olfactory sensory input are known to induce neuroplasticity. Neuron activation, due to olfactory sensory input, activates the immediate early gene c-fos in the olfactory bulb (OB). The presence of fos, the protein derived from c-fos gene expression, can be used to measure changes in OB circuit activity. In the present study, olfactory sensory input was disrupted in mice by intranasal irrigation with the detergent Triton X-100. This induces a temporary loss of the sense of smell, known as anosmia, and a decrease in OB dopamine (DA) concentration. We hypothesized that, due to a Joss of inhibitory DA, Triton X-100 treated mice would have an increase in fos immunopositive cells after odor exposure when compared to control (phosphate buffered saline treated) mice. To test for anosmia induction by Triton X-100, mice underwent a behavioral habituation/dishabituation task twenty-four or forty-eight hours after the final treatment. Both control mice and forty-eight hour recovered Triton X-100 mice displayed normal investigative behavior, indicating they were not anosmic. However, twenty-four hour recovered Triton X-100 mice displayed behavior indicative of anosmia. A separate group of mice were exposed to odor stimulation forty-eight hours after the final treatment, and the OBs were processed for immunohistochemical detection of fos protein. Tissue analysis showed no significant difference in fos immunopositive cell counts between treatment groups