Title: α-Synuclein fibrils induced disruption of pacemaker firing in dopamine neurons is dependent on selective K-ATP channel activation
Host: Ashutosh Dhingra
α-Synuclein fibrils induced disruption of pacemaker firing in dopamine neurons is dependent on selective K-ATP channel activation Parkinson’s disease is associated with α-synuclein aggregation and progressive loss of substantia nigra dopaminergic neurons (SN DA-neurons). Precise mechanism(s) behind selective vulnerability of SN DA-neurons to α-synuclein aggregation in comparison to ventral tegmental area (VTA) DA neurons is not known. Even within SN, DA-neurons in ventro-lateral tier degenerate earlier and to a larger extent compared to the neurons in dorso-medial tier. In our lab we focus on the cellular mechanisms by which α-synuclein aggregates cause toxicity to the cells as well as why different cell populations have different response to them. In my talk, I will focus on the involvement of K-ATP channel as a molecular player in determining α-synuclein’s toxicity to dopaminergic cells.