Signalling pathways involved in the sensitisation of mouse nociceptive neurones by nerve growth factor - PubMed (original) (raw)

A, NGF has no effect on the Ca2+ increase evoked by KCl (25 m

m

, 9 s). B, NGF has no effect on the Ca2+ increase evoked by ATP (100 μ

m

, 15 s). Neurones incubated with thapsigargin (10 μ

m

) for 20 min prior to experiments; the Ca2+ increase evoked by thapsigargin lasted 5–7 min, showing that stores were completely emptied with a 20 min pre-exposure. C, enhancement of TRPV1 function by NGF is observed following complete block of voltage-sensitive ion channels by lidocaine (lignocaine; 2 m

m

, black bar). KCl-evoked Ca2+ increase (see two applications at start) is completely abolished by lidocaine but enhancement of capsaicin-evoked [Ca2+]i increase by NGF is still observed. D, collected results of experiments similar to those in A, B and C, together with experiment similar to C in which thapsigargin (10 μ

m

, applied 20 min prior to experiment) was used to empty subcellular Ca2+ stores. Bars give ±

s.e.m

. Numbers of cells and separate experiments as follows: control, _n_cell = 112, _n_exp = 8; NGF alone, _n_cell = 152, _n_exp = 26; NGF + lidocaine, _n_cell = 60, _n_exp = 8; NGF + thapsigargin, _n_cell = 71, _n_exp = 16; KCl, _n_cell = 88, _n_exp = 7; KCl + NGF, _n_cell = 144, _n_exp = 7; ATP, _n_cell = 23, _n_exp = 9; ATP + NGF, _n_cell = 63, _n_exp = 15.