Parkinson’s disease (PD) causes multiple non-motor symptoms as well as distinctive motor deficits. It is well known that chemosensory and mild cognitive impairments frequently occur in the early stage of PD, but the mechanisms underlying these PD-related prodromal impairments remain unknown. We examined whether intranasal rotenone-administrated male C57BL/6J mouse was a suitable model for elucidation of PD-related prodromal/non-motor symptoms. The 1-week rotenone treatment induced chemosensory and conditioned taste aversion memory impairments without locomotor impairments. Subsequent catecholamine (CA) neuron and fiber loss was observed in the first central nervous system for chemosensory information relays (the olfactory bulb and nucleus of solitary tract) and the critical brain region of taste associative memory (the dysgranular insular cortex) in 1-week rotenone-treated mice, respectively. Despite no apparent changes in the number of CA neuron in the substantia nigra and the ventral tegmental area of 1-week rotenone-treated mice, those of 4-week rotenone-treated mice were significantly reduced (> 70%) at the fifth week. These results suggest that this model employing short-term intranasal rotenone administration will be useful for the elucidating the prodromal stage of PD pathophysiology.