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Table 7 Activation and steady-state inactivation parameters

From: A structural analysis of the splice-specific functional impact of the pathogenic familial hemiplegic migraine type 1 S218L mutation on Cav2.1 P/Q-type channel gating

hCav2.1

Activation V50 (mV)

Activation k

N

Inactivation V50 (mV)

Inactivation k

N

wt ΔSSTR

−11.80 ± 0.46

3.65 ± 0.08

13

−45.06 ± 0.73

6.42 ± 0.12

12

S218L ΔSSTR

−16.78 ± 031***

5.21 ± 0.16***

16

−60.47 ± 0.37***

5.28 ± 0.18**

8

wt +SSTR

−15.44 ± 0.30###

3.99 ± 0.06

17

−47.16 ± 0.64

6.08 ± 0.18

8

S218L +SSTR

−22.05 ± 0.44***

5.70 ± 0.04***

12

−62.90 ± 0.43***

5.24 ± 0.31*

8

  1. Summary table showing mean values ± SEM of activation and inactivation voltage dependence parameters. N = sample size. P values listed below correspond to results from one-way ANOVA with post hoc Tukey test
  2. ***: P value < .0001 indicate statistical significance of S218L mutant voltage dependence values as compared to the corresponding wild type
  3. ###: P value < .0001 from the statistical comparison between activation V50 of wild type channels
  4. **: P = 0.0009 from statistical comparison between S218L ΔSSTR and wt ΔSSTR
  5. The significance level obtained by comparing activation V50 and k values between S218L mutant channels was P < .0001, and P = 0.0108, respectively. The significance level obtained for k values between wild type channels was P = 0.0980
  6. *: P value = 0.0364 from statistical comparison between S218L +SSTR and corresponding wildtype +SSTR
  7. Comparison between the two wild-type isoforms (V50 P = 0.0821; k P = 0.5809) indicates no statistical difference of inactivation parameters. Comparison between the two mutant channels shows no significant difference in V50 (P = 0.0616), or k (P = 0.9993