Neurophysiology of Drosophila Models of Parkinson’s Disease

<table class="figure-group"><tr class="fig-image" id="a"><td><object data="https://static.hindawi.com/articles/pd/volume-2015/381281/figures/381281.fig.002a.svgz" name="381281.fig.002a" type="image/svg+xml"></object></td></tr><tr class="fig-caption"><td>(a) Evoked EJP</td></tr><tr class="fig-image" id="b"><td><object data="https://static.hindawi.com/articles/pd/volume-2015/381281/figures/381281.fig.002b.svgz" name="381281.fig.002b" type="image/svg+xml"></object></td></tr><tr class="fig-caption"><td>(b) Spontaneous mEJP</td></tr></table>

<div>Pink1 mutants display a progressive decline in synaptic transmission under high frequency stimulation. ((a)i-ii) Pink1 (Pink1B9) mutants showed no perturbation to basal neurotransmitter release properties, with no significant difference in the amplitude of evoked excitatory junction potentials (EJP) observed between Pink1 mutants and controls. ((a)iii) Under high frequency stimulation (10 min, 10 Hz) Pink1 mutants showed a substantial, progressive decline in synaptic transmission when compared to controls. ((b)i–iii) Pink1 mutants showed no significant difference in spontaneous miniature EJP (mEJP) amplitude (i-ii) or frequency (i and iii) when compared to controls. Adapted from [<a href="/journals/pd/2015/381281/#B21">21</a>].</div>

Parkinson’s Disease

Neurophysiology of Drosophila Models of Parkinson’s Disease

Figure 2