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. 2006 Aug 31;577(Pt 1):169–190. doi: 10.1113/jphysiol.2006.116418

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.