Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.17.045013v1?rss=1 Authors: Kulkarni, A. S., Cortijo, M. d. M., Roberts, E. R., Suggs, T. L., Stover, H. B., Pena-Bravo, J. I., Steiner, J. A., Luk, K. C., Brundin, P., Wesson, D. W. Abstract: Parkinson's disease (PD) neuropathology is characterized by intraneuronal protein aggregates composed of misfolded -Synuclein (-Syn), as well as degeneration of substantia nigra dopamine neurons. Deficits in olfactory perception and aggregation of -Syn in the olfactory bulb (OB) are observed during early stages of PD, and have been associated with the PD prodrome, before onset of the classic motor deficits. -Syn fibrils injected into the OB of mice cause progressive propagation of -Syn pathology throughout the olfactory system and are coupled to olfactory perceptual deficits. We hypothesized that accumulation of pathogenic -Syn in the OB impairs neural activity in the olfactory system. To address this, we monitored spontaneous and odor-evoked local field potential dynamics in awake wild type mice simultaneously in the OB and piriform cortex (PCX) one, two, and three months following injection of pathogenic preformed -Syn fibrils in the OB. We detected -Syn pathology in both the OB and PCX. We also observed that the presence of -Syn pathology, triggered by -Syn fibril injection, influenced certain oscillatory spectral bands in these regions. These changes in neural activity occurred with region specificity, and in some cases transiently relative to the number of months that had elapsed after injection. Together, we provide evidence that -Syn pathology in the olfactory system impacts in vivo neural activity and provides initial insights into its network-level effects. Copy rights belong to original authors. Visit the link for more info