Our initial studies in this model confirmed multiple neuropathological features similar to that in PD patients and other preclinical models of PD 
. MAO-B elevation caused a significant age-dependent loss of tyrosine hydroxylase (TH) dopaminergic neurons in the substantia nigra. Furthermore, older animals (14 months old) had an enhanced loss of TH+ neurons compared with younger mice (3–4 months old). Increased MAO-B expression also induced elevation in substantia nigra microglia activation. Additionally, anti-oxidant, anti-inflammatory, and MAO-B inhibitor treatment to such animals was found to be neuroprotective, indicating its validity as a model to test therapeutic interventions 
In the present study, we established the parkinsonian behavioral properties of our astrocytic MAO-B transgenic mouse model using multiple behavioral parameters. Initial open field studies showed a 32–35% loss of ambulatory motor function in dox-induced MAO-B mice compared to non-induced MAO-B 
. Similarly, we found treatment and age-dependent decreases in ambulatory function in addition to other behavioral variables (movement, resting and stereotypy) in the open field test. We also saw an age and treatment related increase in hindlimb clasping behavior, which is present in other neurodegenerative and PD mouse models 
. However, we did not see a dox-induced effect in the pole test, but rather identified an age-related effect. Furthermore, these animals did not show a deficit in movement initiation as measured by turning ability in the pole test. Others have identified movement initiation deficit using the forced stepping test in MPTP-treated mice and hemiparkinsonian 6-hydroxydopamine lesioned rats 
. This test is widely used to measure hemispheric differences in unilaterally lesioned rats. It is unclear if the forced stepping test is sensitive in our MAO-B model but, to our knowledge, this specific behavior is not widely utilized in other PD transgenic mouse models. Future studies that evaluate other motor initiation behaviors such as the adhesive removal test 
which are validated in transgenic PD animals may prove to be sensitive in the MAO-B transgenic model. In addition to multiple behavioral deficits in the MAO-B transgenic mouse, we also showed that decreases in DA in the striatum was most severe in aged dox-treated mice, similar to previous reports of PD mouse models 
. Taken together, these studies confirm that the astrocytic MAO-B transgenic model shows age-related neuropathological properties and multiple motor behavioral deficits similar to those exhibited in PD patients and preclinical models.
In conclusion, we demonstrate in the present study that increased expression of astrocytic MAO-B in transgenic mice causes many of the behavioral phenotypes found in other mouse models of PD. Along with our earlier studies in this model, it is clear that increases in astrocyte MAO-B expression is detrimental to neuronal function and can lead to multiple behavioral deficits. These results confirm that this mouse model can be useful to study PD-associated pathophysiology and testing of preclinical therapeutics.