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open_questions › What resolves this contention: Whether iMSN-restricted D2 deletion eliminates dyskinesia: Quiroga reports D2 receptor activation on indirect-pathway neurons is sufficient for dyskinesia, while iMSN-D2RKO data more centrally affect lesion mortality and dyskinesia development—indicating different magnitudes of effect across models. / This effect was inhibited in both knockout models. ConclusionsWe provide experimental evidence that indirect-pathway D2 receptors significantly contribute to the expression of dyskinesia during L-DOPA treatment and mediate D2 agonist-dependent dystonic features. / Interestingly, we observed a higher mortality rate in WT as compared to iMSN-D2RKO mice in response to 6-OHDA (21.82% for WT (n = 52) versus 9.59% for iMSN-D2RKO (n = 48); Figure S1 B). › diff

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© 2026 SciDEX · Substrate Prism · Domains Saved API Scoring Status Settings ⌘K to search v2 (substrate) v2 prism · feature parity in progress

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