Fig. 2
From: Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease

Cav2.3 contributes to somatic action potential-related Ca2+ oscillations in adult mouse SN dopaminergic neurons. a–c Neurons were recorded in the perforated patch-clamp configuration while somatic Ca2+ dynamics were simultaneously imaged (insert a). Left: Continuous recordings of a wildtype SN dopaminergic (DA) neuron (a), Cav2.3 knockout SN dopaminergic neuron (b), and wildtype VTA dopaminergic neuron (c) illustrating the action potential (AP) firing and the associated Ca2+ oscillations. Right: Mean of 20 APs and associated mean Ca2+ oscillations for the neurons from the left. Individual traces are superimposed in grey. d Average spikes (left) and Ca2+ transients (right) of wildtype SN dopaminergic (black trace, n = 15), Cav2.3 knockout SN dopaminergic (red trace, n = 12), and wildtype mesolimbic VTA dopaminergic (blue trace, n = 7) neurons. e Plots showing AP after-hyperpolarizations (AHP, left), peak Ca2+ amplitudes (as ΔRFura,max, middle) and area under the curve (right, AU arbitrary units) of AP-induced Ca2+ transients during pacemaking at ~1.5 Hz. f Remaining AHP and amplitude of the action potential evoked Ca2+ signals (see Methods) in SN dopaminergic neurons of Cav2.3 wildtype (n = 6) and Cav2.3 knockout (n = 8) mice during the presence of 100 nM SNX-482, relative to those before SNX-482 application. This low concentration likely does not completely inhibit Cav2.3 and was used as SNX-482 can inhibit other channels at higher concentrations. A-type K+ currents were blocked throughout the whole experiment by 4 mM 4-AP. Tukey's boxplots are shown. Significances are indicated by asterisks: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Data values and comparison of all AP parameters are detailed in Supplementary Table 6A–D and Supplementary Figs. 1/2. Source data are available as a Source Data file