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| Poster #266 The persistence of changes in olfactory bulb TAAR4-related circuits evoked by early postnatal exposure to phenethylamine (PEA) following olfacotry sensory neuron ablation |
| Jordan D. Gregory1,2 & Claire E. Cheetham1 1Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA, United States 2Center for Neuroscience at the University of Pittsburgh, Pittsburgh, PA, United States |
Critical periods are essential for proper development of mammalian sensory circuits. In the mouse olfactory system there is an early postnatal critical period during which errors in glomerular map formation can be corrected. Furthermore, critical period exposure can alter the valence of innately recognized odorants. Mice exposed during the olfactory critical period to the innately aversive odorant phenethylamine (PEA), detected by olfactory sensory neurons (OSNs) expressing the trace amine-associated receptor 4 (TAAR4) do not demonstrate stereotypical innately avoidant behaviors, but rather are attracted to PEA. This change in behavior is accompanied by an increase in the number of TAAR4 glomeruli per OB. Here, we seek to address two key questions: how neonatal PEA exposure alters the odor responsiveness of OB output neurons, and whether the changes in valence toward PEA persist following complete OSN ablation and subsequent reinnervation. To address the first question, we injected mice with AAV5-syn-GCaMP6s to record PEA-evoked calcium responses in mitral and tufted cells using in vivo 2-photon microscopy. To address the second question, PEA-exposed mice underwent repeated odor preference testing to determine whether the shift in innate valence persists following methimazole (MMZ)-mediated OSN ablation and subsequent repopulation. While we did not see a difference in OB output neuron activity after neonatal PEA exposure, repeated odor preference testing revealed that the preference for PEA does not recover six weeks after MMZ treatment. These data suggest that OB circuitry may reorganize after large-scale OSN ablation and regeneration. |