Galvanic vestibular stimulation down-regulated NMDA receptors in vestibular nucleus of PD model

Parkinsonian symptoms relief by electrical stimulation is known to modulate neural network activity, and Galvanic vestibular stimulation (GVS) has been proposed as an alternative electrical stimulation. However, the underlying mechanism is still elusive. Due to the tight link from the peripheral area to vestibular nucleus (VN), the effect by GVS was investigated to understand the neural mechanism. Using SD rats, behavioral response, extracellular neural recording, and immunohistochemistry of 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 debilitated function of locomotion, and the loss of TH + neurons in mfb and striatum was observed. Sixty-five neuronal extracellular activities (32 canal & 33 otolith) were recorded, and 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 in the PD model, and the effect by GVS was significantly evident in NMDA receptors (p < 0.018). Thus, the increased glutamate receptors in PD models were down-regulated by GVS, and the plastic modulation mainly occurred through NMDA receptor in VN.