Table 2.
Receptor | GABA | 3α5αP | OT1 | Fr OT1 | OT2 | Fr OT2 | OT3 | Fr OT3 | N |
---|---|---|---|---|---|---|---|---|---|
WT | 50 | 0.31 ± 0.14 | 0.20 ± 0.05 | 3.0 ± 0.5 | 0.67 ± 0.06 | 6.3 ± 2.6 | 0.13 ± 0.05 | 7 | |
WT | 50 | 10 | 0.29 ± 0.13 NS | 0.29 ± 0.05* | 3.0 ± 2.6 NS | 0.31 ± 0.11*** | 16.5 ± 6.2** | 0.40 ± 0.09*** | 4 |
mutant | 100 | 0.39 ± 0.03 | 0.80 ± 0.07 | 1.2 ± 0.1 | 0.20 ± 0.07 | — | 0 | 4 | |
mutant | 100 | 10 | 0.53 ± 0.32 NS | 0.24 ± 0.07*** | 5.5 ± 0.5** | 0.61 ± 0.10** | 27.8 ± 10.7 | 0.15 ± 0.08** | 3 |
Receptor | GABA | AP | CT1 | Fr CT1 | CT2 | Fr CT2 | CT3 | Fr CT3 | N |
---|---|---|---|---|---|---|---|---|---|
WT | 50 | 0.19 ± 0.10 | 0.56 ± 0.09 | 1.5 ± 0.6 | 0.15 ± 0.07 | 13.0 ± 3.5 | 0.29 ± 0.06 | 7 | |
WT | 50 | 10 | 0.12 ± 0.01 NS | 0.55 ± 0.07 NS | 1.0 ± 0.3 NS | 0.35 ± 0.07** | 10.7 ± 3.5 NS | 0.10 ± 0.04*** | 4 |
mutant | 100 | 0.24 ± 0.05 | 0.50 ± 0.06 | 1.3 ± 0.5 | 0.14 ± 0.02 | 6.2 ± 2.3 | 0.37 ± 0.04 | 4 | |
mutant | 100 | 10 | 0.18 ± 0.04 NS | 0.81 ± 0.09* | 1.2 ± 0.4 NS | 0.16 ± 0.07 NS | 11.2 ± 6.1 NS | 0.04 ± 0.03*** | 3 |
Single-channel activity in clusters of openings was analysed to determine the numbers of components present, and their mean durations and overall fraction of the total events. Mean values are presented for the mean open time durations (OT1, OT2 and OT3) and the fractions of the total number of openings in each component. The longest duration component (OT3) was not present for activity from the mutant receptor in the absence of 3α5αP, as is also true for receptors including the α1(Q241L) subunit (Akk et al. 2008), but appeared in the presence of 3α5αP. The longest duration closed time component (CT3) was significantly less common in the presence of 3α5αP. (Significance of the difference between control and +3α5αP by two-tailed t test for each receptor type; NS P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001.) We compared the ability of kinetic models to describe the data by comparing the log-likelihoods for the respective fits (Horn, 1987). We fit open time distributions with either 2 or 3 open states, for both control (no 3α5αP) and plus steroid for responses from α1(I&L) +β2(TM1) +γ2L receptors. The differences in log-likelihood values for control recordings were 0, 4, 2 and 1 unit, while for recordings plus steroid they were 10, 11 and 16. For an assumed probability of 0.05 that the increased log-likelihood would arise by chance, the difference in log-likelihood for each added state should be greater than 3. We conclude that a 3 open state model does not provide a significantly better description for control records, but does for recordings in the presence of steroid.