1. Dopamine Induces Oscillatory Activities in Human Midbrain Neurons with Parkin Mutations 
Ping Zhong, Zhixing Hu, Houbo Jiang, Zhen Yan, Jian Feng 
Cell Reports 
Volume 19, Issue 5, Pages (May 2017)
DOI: /j.celrep
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2. Cell Reports 2017 19, 1033-1044DOI: (10.1016/j.celrep.2017.04.023)
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3. Figure 1
Differentiation of Patient-Specific iPSCs to a Mixed Population of Midbrain Neurons
(A–D) Phase contrast images of iPSCs (A) being differentiated to embryoid bodies (B), neuroepithelial cells (C), and neurons (D).
(E–S) Costaining of iPSC-derived neurons for the DA marker tyrosine hydroxylase (TH) (E, H, K, N, and Q), the GABAergic neuronal marker GABA (F), the glutamatergic neuronal marker vGlut2 (I), dopamine D1 receptor (D1R) (L), dopamine D2 receptor (D2R) (O), the midbrain marker FoxA2 (R), and DNA for merged images as indicated (G, J, M, P, and S). Scale bars, 100 μm.
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4. Figure 2
The Effects of Dopamine on sEPSCs in iPSC-Derived Neurons from Normal Subjects and PD Patients with Parkin Mutations
(A and B) Normalized plots of sEPSC amplitude (A) and frequency (B), showing the effect of dopamine (100 μM) in iPSC-derived neurons from parkin patients versus normal subjects. Inset: bar graph (mean ± SEM) summary shows the percentage change by dopamine in two groups of neurons (∗p < 0.05 versus normals).
(C and D) Representative traces of sEPSCs at different time points (indicated by the numbers in A and B plots) in iPSC-derived neurons from a parkin patient (C) versus a normal subject (D).
(E and F) Blocking non-NMDA ionic glutamate receptors with DNQX (50 μM) abolished sEPSCs in neurons from parkin patients (E) and normal subjects (F).
(G–J) Miniature EPSCs (mEPSCs) in patient (G) or normal (H) neurons treated with vehicle or dopamine (100 μM) had similar amplitudes (I) and frequencies (J).
(K) Quantal content of sEPSCs as measured by dividing the sEPSC amplitude by mEPSC amplitude in neurons from normal subjects and parkin patients treated with vehicle or dopamine (100 μM) (∗p < versus normals).
See also Figure S1.
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5. Figure 3
All the Effects of Dopamine on sEPSCs Are Blocked by Co-application of D1-Class and D2-Class Antagonists
(A and B) Normalized plots of sEPSC amplitude (A) and frequency (B), showing the effect of dopamine (100 μM) in the presence of SCH23390 (10 μM) and sulpiride (20 μM) in iPSC-derived neurons from parkin patients versus normal subjects. Inset: bar graph (mean ± SEM) summary shows the percentage change by dopamine in the presence of SCH23390 and sulpiride in two groups of neurons.
(C and D) Representative traces of sEPSCs at different time points (indicated by the numbers in A and B plots) in iPSC-derived neurons from a parkin patient (C) versus a normal subject (D).
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6. Figure 4
The Effect of Dopamine in the Presence of a D1-Class Antagonist
(A and B) Normalized plots of sEPSC amplitude (A) and frequency (B), showing the effect of dopamine (100 μM) in the presence of the D1-class antagonist SCH23390 (10 μM) in iPSC-derived neurons from parkin patients versus normal subjects. Inset: bar graph (mean ± SEM) summary shows the percentage change by dopamine in the presence of SCH23390 in two groups of neurons.
(C and D) Representative traces of sEPSCs at different time points (indicated by the numbers in A and B plots) in iPSC-derived neurons from a parkin patient (C) versus a normal subject (D).
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7. Figure 5
When D2-Class Receptors Are Blocked, Dopamine Induces Rhythmic Bursting of sEPSCs in iPSC-Derived Neurons from Parkin Patients
(A and B) Normalized plots of sEPSC amplitude (A) and frequency (B), showing the effect of dopamine (100 μM) in the presence of the D2-class antagonist sulpiride (20 μM) on iPSC-derived neurons from parkin patients versus normal subjects.
(C and D) Representative traces of sEPSCs in iPSC-derived neurons from a parkin patient (C) versus a normal subject (D). Inset in (C) shows the expanded view of sEPSCs during bursting.
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8. Figure 6
Application of D1-Class Agonist Induces Rhythmic Bursting of sEPSCs in iPSC-Derived Neurons from Parkin Patients
(A and B) Normalized plots of sEPSC amplitude (A) and frequency (B), showing the effect of the D1-class agonist SKF81297 (20 μM) on iPSC-derived neurons from parkin patients versus normal subjects.
(C and D) Representative traces of sEPSCs from iPSC-derived neurons from a parkin patient (C) versus a normal subject (D). Inset in (C) shows the expanded view of sEPSCs during bursting.
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9. Figure 7
Rhythmic Bursting of sEPSCs in Parkin-Deficient Neurons Was Rescued by Wild-Type, but Not Mutant, Parkin
(A and B) Normalized sEPSC amplitude (A) and frequency (B) for P002 neurons transduced with lentiviruses expressing parkin, T240R mutant parkin, or GFP.
(C–E) Representative traces of sEPSCs from P002 neurons transduced with lentiviruses expressing parkin (C), T240R mutant parkin (D), or GFP (E).
(F) A model for oscillatory activities in neurons from parkin patients in response to D1 receptor activation. Details are in the Discussion.
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