Table 2.
Ca2+ transients in subpopulations of medium-diameter DRG neurons
Subpopulation | n | Δ[Ca2+]i (nm) | T50 (s) |
---|---|---|---|
IB4+ | 96 | 331 ± 29** | 8.9 ± 1.2** |
IB4− | 31 | 113 ± 11 | 3.5 ± 0.3 |
CAP+ | 85 | 319 ± 31** | 8.2 ± 1.1 |
CAP− | 42 | 166 ± 29 | 5.5 ± 1.5 |
IB4+/CAP+ | 65 | 344 ± 32 | 8.6 ± 1.3 |
IB4+/CAP− | 31 | 271 ± 71 | 10.3 ± 4.1 |
IB4−/CAP+ | 20 | 115 ± 26 | 5.1 ± 1.1 |
IB4−/CAP− | 11 | 113 ± 13 | 3.0 ± 0.2 |
The magnitude (Δ[Ca2+]i) and decay (T50) of high-K+-evoked Ca2+ transients were analysed in subpopulations of medium-diameter (i.e. 30–40 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 magnitude was significantly larger
P < 0.01 and 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 < 0.01) larger in CAP+ neurons than that in CAP– neurons. There was a significant (P < 0.01) group effect in the magnitude of evoked Ca2+ transients when subpopulations defined by the combination of IB4 binding and CAP sensitivity were compared. Post hoc analysis (Tukey test) indicated that the magnitude of the transient in IB4+/CAP+ neurons was significantly larger than that in IB4–/CAP + (P < 0.05) and IB4–/CAP– neurons (P < 0.01). There were no other significant differences between groups.