Fig. 2: AIMs score and synaptic plasticity in 6-OHDA Models. | npj Parkinson's Disease

Fig. 2: AIMs score and synaptic plasticity in 6-OHDA Models.

From: Molecular and cellular determinants of L-Dopa-induced dyskinesia in Parkinson’s Disease

Fig. 2

A Left: AIMs scores analysis of all session times. Right: evaluation of AIMs distinct components, limb, axial and orolingual. B AIMs scores analysis of Partial rats 3 W (dark blue circle) and Partial rats 6 W (light blue circle) treated with L-Dopa (Two-way ANOVA Partial rats 3 W vs. Partial rats 6 W, Interaction: F(8,1197) = 1.170, P > 0.05 Bonferroni’s post-hoc test). Right: evaluation of AIMs distinct components in both experimental groups (unpaired t-test for limb, axial and orolingual of Partial rats 3 W vs. Partial rats 6 W, P > 0.05). C Effect of L-Dopa treatment on corticostriatal LTP and synaptic depotentiation of SPNs. Left: Time course of EPSPs amplitude in response to HFS (n = 6, paired t-test pre- vs. post‐HFS, t = 8.671, df = 9, ***P < 0.001) and LFS (n = 6, paired t-test post‐HFS vs. post‐LFS, t = 1.013, df = 6, P > 0.05) protocols in Full +3W L-Dopa (green circle). Green solid line shows EPSPs amplitude in response to HFS in SPNs of Full model without treatment (C) Right: Time course of EPSPs amplitude in response to HFS (n = 5, paired t-test pre- vs. post‐HFS, t = 12.190, df = 9, ***P < 0.0001) and LFS (n = 5, paired t-test post‐HFS vs. post‐LFS, t = 11.570, df = 7, ###P < 0.0001) protocols. The blue solid line shows EPSP amplitude in response to HFS in SPNs of the Partial model without treatment. Representative traces of EPSPs from SPNs before (baseline) and after HSF and LFS. The scale bar is 5 ms/10 mV for all traces. D Linear regression and correlation analysis between the depotentiation, expressed as % change of EPSP amplitude and AIMs score (Coefficients of correlation: r = 0.892, F (1,8) = 65.88, ***P < 0.001) in 6-OHDA- Full and -Partial Models following a chronic 3 week L-Dopa administration.

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