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- W3044337628 abstract "Changes in striatal cholinergic interneuron (ChI) activity are thought to contribute to Parkinson's disease pathophysiology and dyskinesia from chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment, but the physiological basis of these changes is unknown. We find that dopamine lesion decreases the spontaneous firing rate of ChIs, whereas chronic treatment with L-DOPA of lesioned mice increases baseline ChI firing rates to levels beyond normal activity. The effect of dopamine loss on ChIs was due to decreased currents of both hyperpolarization-activated cyclic nucleotide-gated (HCN) and small conductance calcium-activated potassium (SK) channels. L-DOPA reinstatement of dopamine normalized HCN activity, but SK current remained depressed. Pharmacological blockade of HCN and SK activities mimicked changes in firing, confirming that these channels are responsible for the molecular adaptation of ChIs to dopamine loss and chronic L-DOPA treatment. These findings suggest that targeting ChIs with channel-specific modulators may provide therapeutic approaches for alleviating L-DOPA-induced dyskinesia in PD patients." @default.
- W3044337628 created "2020-07-29" @default.
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- W3044337628 date "2020-07-20" @default.
- W3044337628 modified "2023-10-03" @default.
- W3044337628 title "Alterations in the intrinsic properties of striatal cholinergic interneurons after dopamine lesion and chronic L-DOPA" @default.
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- W3044337628 doi "https://doi.org/10.7554/elife.56920" @default.
- W3044337628 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7380940" @default.
- W3044337628 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32687053" @default.
- W3044337628 hasPublicationYear "2020" @default.
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