Article: Dysfunctional Calcium and Glutamate Signaling in Striatal Astrocytes from Huntington's Disease Model Mice.

Table 3.

TBOA has a greater effect on astrocyte EFS-evoked iGluSnFR signals in WT mice than in R6/2 mice

	Control	+ TBOA	p	Fold-change from control to TBOA	n (cells, mice)
WT
Peak dF/F	0.41 ± 0.09	1.07 ± 0.09	<0.00001	7.0 ± 1.4	21, 4
Decay (s)	2.79 ± 0.55	10.85 ± 1.24	<0.00001	7.2 ± 2.1	21, 4
Area (dF/F · s)	0.73 ± 0.14	5.18 ± 0.56	<0.00001	10.3 ± 2.2	21, 4
R6/2
Peak dF/F	0.42 ± 0.05	0.54 ± 0.05	0.00025	1.8 ± 0.2	25, 4
Decay (s)	5.55 ± 0.40	12.77 ± 1.88	0.00037	2.5 ± 0.4	25, 4
Area (dF/F · s)	1.20 ± 0.09	3.13 ± 0.53	0.00146	2.5 ± 0.4	25, 4

Data are from experiments such as those illustrated in Figure 7C, but summarized here for R6/2 and noncarrier controls (WT). TBOA significantly increased the EFS-evoked iGluSnFR signals in WT and R6/2 mice, but the fold changes were significantly greater in WT mice for all three comparisons of peak δF/F (p = 0.00132), decay time (p = 0.01696), and area (p = 0.00296) between WT and R6/2 mice. The mean values for fold changes calculated from individual experiments are shown.

Inferred neuron-electrophysiology data values

Neuron Type	Neuron Description	Ephys Prop	Extracted Value	Standardized Value	Content Source