Olfactory dysfunction is an early symptom of neurodegenerative diseases, including Parkinson’s disease (PD) and multiple sclerosis (MS). Recent data showed that 30-40% MS patients and 90 % PD patients experience olfactory dysfunction. Studies have shown that adenosine signaling has a pivotal role in olfactory processing; thus, deciphering the changes in adenosine signaling may be crucial for understanding the disease pathogenesis. Aim of this study was to characterize olfactory dysfunction from the aspect of adenosine metabolism, focusing on ecto-5’ nucleotidase (CD73) in the olfactory bulb (OB). To induce the model of MS, experimental autoimmune encephalomyelitis (EAE), we used male 2 month-old Dark Agouti rats and immunized them with spinal cord homogenate in complete Freund’a adjuvant with Mycobacterium tuberculosis. Next, we injected 6-hydroxydopamine (6-OHDA) into substantia nigra pars compacta of male 2 month-old Wistar rats to induce the model of PD. We performed enzyme assays to examine CD73 activity in OB of EAE and 6-OHDA animals; 6-OHDA animals showed a statistically significant change in CD73 activity at both 3- and 5-day post injection (dpi), while at 7-dpi, enzyme activity remained at the control level. EAE animals in the peak of the disease (11-13-dpi) did not show a statistically significant change in CD73 activity. Thus, we conclude that the rate of adenosine production is altered in 6-OHDA in early phase of the disease, indicating an importance of further examinations.