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Striatal Dopamine Transporter Function Is Facilitated by Converging Biology of α-Synuclein and Cholesterol. | LitMetric

AI Article Synopsis

Article Abstract

Striatal dopamine transporters (DAT) powerfully regulate dopamine signaling, and can contribute risk to degeneration in Parkinson's disease (PD). DATs can interact with the neuronal protein α-synuclein, which is associated with the etiology and molecular pathology of idiopathic and familial PD. Here, we tested whether DAT function in governing dopamine (DA) uptake and release is modified in a human-α-synuclein-overexpressing (-OVX) transgenic mouse model of early PD. Using fast-scan cyclic voltammetry (FCV) in acute striatal slices to detect DA release, and biochemical assays, we show that several aspects of DAT function are promoted in -OVX mice. Compared to background control α-synuclein-null mice (-null), the -OVX mice have elevated DA uptake rates, and more pronounced effects of DAT inhibitors on evoked extracellular DA concentrations ([DA]) and on short-term plasticity (STP) in DA release, indicating DATs play a greater role in limiting DA release and in driving STP. We found that DAT membrane levels and radioligand binding sites correlated with α-synuclein level. Furthermore, DAT function in -null and -OVX mice could also be promoted by applying cholesterol, and using Tof-SIMS we found genotype-differences in striatal lipids, with lower striatal cholesterol in -OVX mice. An inhibitor of cholesterol efflux transporter ABCA1 or a cholesterol chelator in -OVX mice reduced the effects of DAT-inhibitors on evoked [DA]. Together these data indicate that human α-synuclein in a mouse model of PD promotes striatal DAT function, in a manner supported by extracellular cholesterol, suggesting converging biology of α-synuclein and cholesterol that regulates DAT function and could impact DA function and PD pathophysiology.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8081845PMC
http://dx.doi.org/10.3389/fncel.2021.658244DOI Listing

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