Аннотация:Introduction: Astrocyte dysfunction is the common pathology resulting in failure of astrocyte-neuron interaction in neurological diseases, including Parkinson's disease (PD). The aim of present study was to evaluate the impact of astrocytic dysfunction caused by striatal injections of selective glial toxin L-aminoadipic acid (L-AA) on the rats locomotor activity in normal conditions and under alpha-methyl-p-tyrosine depletion of catecholamines synthesis.Materials and Methods:Thirty three male Wistar rats were used in the experimient. Intrastriatal L-AA injections (100 μg) were performed into the right striatum. Alpha-methyl-p-tyrosine (a-MT, 100 mg/kg, inhibitor of tyrosine hydroxylase) was intraperitoneally injected for catecholamine depletion. The animals were divided into five groups: 1) L-AA treated (n=7), 2) L-AA+a-MT treated (n=5), 3) Sham operated (n=7), 4) Sham+a-MT treated (n=5), 5) Intact control (n=9). For assessment of motor function, open field and beam walking test were used on 3rddayafter operation.Neuronal and astrocyte markers (glial fibrillary acidic protein, glutamine synthetase, tyrosine hydroxylase, neuronal nuclear antigen) was examined in the striatim by immunohistochemistry.Results.Administration of L-AA led to astrocyticdegeneration in the striatum. No neuronal death and disruption of dopaminergic terminals were detected. The distance traveled by L-AA and a-MT-treated animals was significantly (p=0.047) shorter compared to sham operated group that was injected with a-MT.In the walking beam test the number of unilateral paw slippings was significantly (p<0.01) higher in L-AA-treated group in compare to sham operated animals. Administration of a-MT alone and together with L-AA did not changes rats perfomance in walking beam test. Conclusion. Astrocyte ablation in dopamine depleted striatum resulted in reduced motor activity and asymmetrical gait disturbances. These findings demonstrate a role of astroglia in motor function regulation in the nigrostriatal system and suggest the possible association of glial dysfunction with motor dysfunction in PD.