Figure 10.

Effects of TEA (10 mM) and 4-AP (5 mM) on MIT following treatment with a high concentration of penitrem A (3 μM; a) or a combination of drugs designed to suppress possible effects of transmitter release from nerve endings (b). (a) Penitrem A applied over 15 min (Pen A; n=21 strips from 16 animals) had no significant effect on MIT when compared to the effect of 0.6% DMSO (Veh; n=18 strips from 15 animals). In the presence of penitrem A, both TEA (TEA+Pen A; n=7 strips from seven animals) and 4-AP (4-AP+Pen A; n=10 strips animals from nine animals) caused increases in MIT, which were similar to those recorded in tissues in the presence of TEA (TEA; n=4 strips from four animals) and 4-AP (4-AP; n=4 from four animals) alone, respectively. ^*MIT during treatment with TEA or 4-AP was significantly different (P<0.05) compared with time/vehicle controls. (b) Following treatment with capsaicin (10 μM) for 20 min, tissues were washed in PSS for 15 min, and then phentolamine, propranolol and atropine (all 1 μM) were added to the bath. MIT during the next 15 min was not significantly different from that recorded prior to capsaicin addition (bar labelled ‘antagonists', n=17 strips from 13 animals). Subsequent addition of either TEA (antagonists+TEA; n=4 strips from n=4 animals) or 4-AP (antagonists+4-AP; n=4 strips from n=4 animals) caused increases in MIT similar to that observed in tissue strips which had not been pretreated (compare with, for example, Figure 10a). ^*MIT during treatment with TEA or 4-AP was significantly different (P<0.05) compared with time/vehicle controls (antagonists+Veh, n=9 strips from n=4 animals).