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. 2010 Oct 6;104(6):3009–3020. doi: 10.1152/jn.00466.2010

Fig. 5.

Fig. 5.

PINK1-deficient SNC dopamine neurons display hyperexcitability in ex vivo brain slice and in vivo. A and B: PINK1-deficient neurons show a greater propensity to fire in a “bursting” manner when treated with N-methyl-d-aspartate (NMDA) ex vivo compared with wild type neurons. Moreover, treatment with the SK channel facilitator, 1-EBIO, can dampen excitability in PINK1-deficient neurons and prevent onset of bursts. (Scale bars: 10 mV, 2 s) C: comparison of extracellular recordings in vivo shows that SNC dopamine neurons from PINK1-deficient mice have similar firing rates to wild type neurons (D) but are often more irregular (E) and show a greater percentage of spikes in bursts (F). (Scale bars: firing pattern, 0.5 mV, 1 s; action potential waveform, 0.5 mV, 1 ms). *, P < 0.05.