Parkinson’s disease (PD) is a neurodegenerative disorder that does not develop spontaneously in some animal species. PD can be induced experimentally in some laboratory animals including mouse, rat and horse. Globus pallidus (GP) and substantia nigra pars compacta (SNc) are damaged in patients with PD. The hallmark of PD is a progressive impaired control of movement, an alteration of autonomic functions, cognitive disorders, behavioral changes, and dementia. Loss of basal forebrain nucleus cholinergic neurons, appearance of Lewy bodies, reduced striatal dopamine, norepinephrine and 5-HT contents, loss of glutamate decarboxylase, leu- and met-enkephalins, and substance-P have been observed in SNCc and ventral tegmentum (VTM) in PD. In order to study the possible changes of field potentials of striatal neurons in the experimental model of PD, 20 male NMRI rats (200-250 g) were used and two guide cannulae (0.7 mm in diameter) were implanted bilaterally into SNC and a bipolar metal wire electrode were implanted into the striatum under stereotaxic surgery. The striatal electrical activity was amplified and recorded. To induce the model of Parkinson’s disease, halopridole (10 µg/µl /rat in each hemisphere) was injected into SNC bilaterally and 25 minutes after injection, striatal local EEG was recorded. EEG amplitude changes were analyzed statistically. Results showed that amplitude of striatal local EEG significantly (P<0.01) decreases after injection of halopridole in SNC. These data suggest that in patients with PD, electrical activity of striatal neurons reduces and, thereby it may reduce the activity of GP neurons.