Figure 6. Loss of α-synuclein (αSyn) impairs short-term plasticity of the cortico-BLA inputs.

(A1) Representative cortico-basolateral amygdala (BLA) excitatory postsynaptic currents (EPSCs) traces from control and preformed fibrils (PFF)-injected mice in response to repetitive stimulation (300 stimuli at 12.5 Hz). (A2) Summarized graph showing the temporal profiles of cortico-EPSCs depression in slices from control and PFFs-injected mice. The cortico-BLA EPSCs from PFFs-injected mice exhibited greater reduction in the amplitude toward the end of repetitive stimulation. n=13–15 neurons/ 3 mice. (B1) Representative cortico-BLA EPSCs traces from wild type (WT) control and αSyn KO mice in response to repetitive stimulation (300 stimuli at 12.5 Hz). (B2) Summarized graph showing the temporal profiles of cortico-EPSCs depression in slices from WT control and αSyn KO mice (n=8–9 neurons/3 mice. *, p<0.05, MWU followed by Bonferroni-Dunn correction for multiple comparisons).

Figure 6—figure supplement 1. α-synuclein (αSyn) KO does not affect short term plasticity profiles of thalamo-BLA inputs.

(A1) Representative thalamo-basolateral amygdala (BLA) excitatory postsynaptic currents (EPSCs) traces from wild type (WT) control and αSyn KO mice in response to repetitive stimulation (300 stimuli at 12.5 Hz). (A2) Summarized graph showing the temporal profiles of thalamo-BLA EPSCs depression in slices from WT control and αSyn KO mice (n=9 neurons/3 mice. No statistical significance was detected between groups, MWU followed by Bonferroni-Dunn correction for multiple comparisons).