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Fig. 1 | Journal of Biomedical Science

Fig. 1

From: An electrophysiological perspective on Parkinson’s disease: symptomatic pathogenesis and therapeutic approaches

Fig. 1

MC drive and major currents involved in the generation and shaping STN bursts. A Top, Membrane hyperpolarization (e.g. in a dopamine-deprived state) facilitates the burst mode of discharges in STN neurons. Bottom, A schematic drawing shows that intrinsic h currents in STN neurons could be insufficient to sustain autonomous burst discharges. The gradual depolarization phase in STN bursts very much relies on the glutamatergic currents provided by the input from the hyperdirect (corticosubthalamic) pathway. This endows STN bursts a strong relay feature for the MC-STN information flow. Once the membrane potential is depolarized enough to bring the T-type Ca2+ channels into a positive feedback activation cycle, the membrane potential is rapidly depolarized and positive-feedback activation of Na+ channels is involved to fire spikes. The burst plateau would sustain until enough “slow” K+ channels, like ERG channels, are opened to repolarize the membrane to a marked hyperpolarized level. B and C In-vitro slice recordings show that STN burst discharges are abolished by CNQX (20 μM) whether the bursts are spontaneous (part B, from a 68-day-old normal male Wistar rat) or evoked by optogenetic stimulation directly on the motor cortex (part C, from a 40-day-old Thy1-ChR2-EYFP transgenic C57BL/6 mouse). The generation of STN bursts thus is not so autonomous, and the glutamatergic input from MC seems to be an absolute requirement in most cases. Refer to Huang et al. 2021 [50] for details of experimental methods and analysis

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