Table 1.
Ca2+ transients in subpopulations of small-diameter DRG neurons
| Subpopulation | n | Δ[Ca2+]i (nm) | T50 (s) |
|---|---|---|---|
| IB4+ | 96 | 445 ± 52 | 12.4 ± 0.9** |
| IB4− | 31 | 416 ± 21 | 6.2 ± 0.5 |
| CAP+ | 85 | 395 ± 19* | 10.8 ± 0.9 |
| CAP− | 42 | 482 ± 45 | 11.1 ± 1.3 |
| IB4+/CAP+ | 65 | 397 ± 20 | 12.0 ± 1.2 |
| IB4+/CAP− | 31 | 458 ± 50 | 13.2 ± 1.6 |
| IB4−/CAP+ | 20 | 390 ± 57 | 6.7 ± 0.7 |
| IB4−/CAP− | 11 | 548 ± 97 | 5.2 ± 0.7 |
The magnitude (Δ[Ca2+]i) and decay (T50) of high-K+-evoked Ca2+ transients were analysed in subpopulations of small-diameter (i.e. < 30 μm) DRG neurons. Subpopulations were defined by IB4 binding, capsaicin (CAP) sensitivity, or the combination of the two and differences between groups (i.e. IB4+versus IB4–) were assessed. The decay of evoked Ca2+ transients was significantly
P < 0.01 slower in IB4+ neurons than in IB4– neurons. The magnitude of the evoked Ca2+ transient was significantly
P < 0.05 smaller in CAP+ neurons than that in CAP– neurons. There was a significant (P < 0.01) group effect in the decay of evoked Ca2+ transients when subpopulations defined by the combination of IB4 binding and CAP sensitivity were compared. Post hoc analysis indicated that the decay of the transient in IB4+/CAP– neurons was significantly slower than that in IB4–/CAP+ (P < 0.05) and IB4–/CAP– neurons (P < 0.05). There were no other significant differences between groups.