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. 2004 May 20;142(2):257–266. doi: 10.1038/sj.bjp.0705778

Figure 2.

Figure 2

Effect of antagonists and CAP pretreatment on WIN-2-evoked CGRP release: the dependence of WIN-2-evoked CGRP release on TRPV1 was assessed using CPZ or I-RTX (a). In addition, the potential role of CB1 receptors was evaluated using AM251 (b) or SR141716A (c), while that of EDG or P2Y receptors was evaluated using suramin (d). The dependence of WIN-2-evoked CGRP release on non-TRPV1 cationic channels was evaluated using the nonspecific calcium channel blocker ruthenium red (e). (f) To examine the potential for CAP to desensitize the WIN-2 response, TG neurons were pretreated with the indicated concentrations of CAP or vehicle for 10 min after which the release buffer was removed and reserved for CGRP analysis and then replaced with fresh buffer. Following 5 min, vehicle or WIN-2 (final concentration of 50 μM) in release buffer was added for 10 min. Both the CAP pretreatment and WIN-2 treatments were assayed for CGRP release. Clear bars indicate CAP-evoked CGRP release and gray bars illustrate the subsequent WIN-2-evoked CGRP response (n=6, ***P<0.001 vs no drug control, #P<0.5 vs WIN-2 50 μM without CAP pretreatment; no comparisons were made for CAP pretreatment only).