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. Author manuscript; available in PMC: 2015 Mar 20.
Published in final edited form as: Curr Biol. 2012 May 24;22(12):1102–1108. doi: 10.1016/j.cub.2012.04.018

Figure 3. Homeostatic Increase in Ca2+ Influx at cacTS2 Mutant Synapses.

Figure 3

(A) Representative traces of spatially-averaged Ca2+ transients of the indicated genotypes (average of 8–12 scans each).

(B) ΔF/F Ca2+ transient peak amplitudes (average and cumulative frequency plot) of control (n=31 boutons; gray), cacTS2 (n=32; light blue), and cacTS2; GluRIIASP16 (n=32; dark blue). All data were collected at room temperature. The peak amplitudes of cacTS2 mutants, and cacTS2; GluRIIASP16 double mutants were smaller than in control (both p<0.004), and there was a significant difference in peak amplitude between cacTS2 mutants, and cacTS2; GluRIIASP16 (p=0.007). Note that cacTS2; GluRIIASP16 double mutants display normal synaptic homeostasis at room temperature (see D) (Frank et al., 2006).

(C) Average baseline fluorescence (‘Fbase’) and decay time constant (‘τ’) of the groups introduced in (B).

(D) Average mEPSP amplitude (‘mEPSP’), Ca2+-transient peak amplitude of (‘ΔF/F’), and quantal content of cacTS2; GluRIIASP16 double mutants normalized to cacTS2. Electrophysiology data is based on a separate set of experiments (control: n=13; cacTS2: mEPSP=1.0±0.01 mV; EPSP=42.9±1.8 mV, n=15; cacTS2; GluRIIASP16: mEPSP=0.44±0.03 mV; EPSP=43.6±4.0 mV, n=8).

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