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. Author manuscript; available in PMC: 2023 Jul 24.
Published in final edited form as: J Neurol Sci. 2022 Feb 23;435:120198. doi: 10.1016/j.jns.2022.120198

Fig. 2.

Fig. 2.

Summary of ET pathophysiology. (A) Climbing fiber overgrowth and hyperinnervation. Reduction of GluRδ2 protein in the Purkinje cells causes climbing fiber synaptic pruning deficits, which lead to hypersynchrony and excessive oscillations in Purkinje cells. (B) Increased inferior olive automaticity and synchrony. β-carboline alkaloids, such as harmaline, lead to augmented T-type calcium channel function and potentially increased inferior olive synchrony via gap junctions. (C & D) GABA dysregulation. GABA receptor knockout in Purkinje cells and reduced GABA receptors in the deep cerebellar nucleus can lead to abnormal oscillations in the circuitry. DCN: deep cerebellar nucleus; IO: inferior olive; PC: Purkinje cell.