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. 2014 Dec 31;113(6):1697–1711. doi: 10.1152/jn.00752.2014

Fig. 1.

Fig. 1.

The Parkinson's disease (PD)-like dopamine (DA) neuron loss pattern and the l-3,4-dihydroxyphenylalanine (l-dopa)-induced phosphorylated extracellular signal-regulated kinase (pERK) in the striatum in Pitx3Null mice. A: tyrosine hydroxylase (TH)-immunostained DA neurons in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). Note the dense DA dendritic network in the substantia nigra pars reticulate (SNr) in Pitx3WT (wild-type) mice (n = 3). B: TH-immunostained DA neurons in the SNc and VTA in Pitx3Null mice (n = 3). Note that the vast majority of the SNc DA neurons and DA dendrites are lost in Pitx3Null mice. A and B are 5-μm confocal optical sections obtained with a ×20 objective under an identical scanning condition. C, C1–C3: extremely dense DA axons in the entire striatum in Pitx3WT mice, but there was no detectable pERK signal. C1: TH. C2: pERK. C3: overlay. AC, anterior commissure; OT, olfactory tubercle. D, D1–D3: extremely severe (>95%) DA axon loss and a robust pERK signal in the dorsal striatum in Pitx3Null mice. D1: TH. D2: pERK. D3: overlay. The pERK signal was exclusively in striatonigral neurons (dual-labeling data not shown). The middle striatum has a significant amount of residual DA axons but no detectable pERK signal. The boxed areas are displayed at a higher magnification at the bottom to show DA axons and pERK-positive cells in Pitx3Null mice. For C and D, drug-naive mice were injected intraperitoneally with 10 mg/kg l-dopa and 5 mg/kg benserazide (3 Pitx3WT mice and 3 Pitx3Null mice). Thirty minutes later, these mice were perfused under deep urethane anesthesia, and brain sections were processed. Each image is a 3-μm confocal optical section obtained with a ×20 objective under an identical scanning condition.