Parkinsonian symptoms relief by electrical stimulation is constructed by modulating neural network activity, and Galvanic vestibular stimulation (GVS) is known to affect the neural activity for motor control by activating the vestibular afferents. However, its underlying mechanism is still elusive. Due to the tight link from the peripheral vestibular organ to vestibular nucleus (VN), the effect by GVS was investigated to understand the neural mechanism. Using Sprague Dawley (SD) rats, behavioral response, extracellular neural recording, and immunohistochemistry in VN were conducted before and after the construction of Parkinson’s disease (PD) model. Animals’ locomotion was tested using rota-rod, and single extracellular neuronal activity was recorded in VN. The immunohistochemistry detected AMPA and NMDA receptors in VN to assess the effects by different amounts of electrical charge (0.018, 0.09, and 0.18 coulombs) as well as normal and PD with no GVS. All PD models showed the motor impairment, and the loss of TH⁺ neurons in medial forebrain bundle (mfb) and striatum was observed. Sixty-five neuronal extracellular activities (32 canal & 33 otolith) were recorded, but no significant difference in the resting firing rates and the kinetic responding gain were found in the PD models. On the other hand, the numbers of AMPA and NMDA receptors increased after the construction of PD model, and the effect by GVS was significantly evident in the change of NMDA receptors (p < 0.018). In conclusion, the increased glutamate receptors in PD models were down-regulated by GVS, and the plastic modulation mainly occurred through NMDA receptor in VN.