Fig. 2

Schematic illustration of DBS suppressing abnormal burst firing in the STN. Under normal conditions, STN neurons are capable of transition between single-spike firing and burst firing by activating distinct sets of ion channels based on the membrane potential state [63]. However, in PD, dopamine deficiency results in relative membrane hyperpolarization, facilitating burst firing in the STN [64, 65]. This abnormal burst firing pattern is closely associated with the manifestation of parkinsonian symptoms [66,67,68]. HFS-DBS induces a transient depolarization of the neuronal membrane. Subsequently, it effectively blocks voltage-gated currents, with a notable impact on T- and L-type Ca²⁺ currents as well as Ca²⁺-activated inward currents. This suppression of abnormal burst firing in the STN contributes to the amelioration of PD symptoms [60, 73]