Figure 1

Stimulated calcitonin gene-related peptide (CGRP) release from single mouse brainstem slices. A) Potassium-induced depolarisation for 5 min induced CGRP release in a reversible manner (n = 11). In adjacent slices, no CGRP release was observed by the same stimulation in the absence of calcium. B) Capsaicin-induced stimulation of CGRP release. The second stimulation induced less CGRP release (n = 11). In the presence of the TRPV1 antagonist BCTC 100 nM (duration indicated by black bar, closed symbols, n = 8) capsaicin-induced release was abolished. C) Acidic extracellular solution of pH 5.8 stimulated CGRP release from brainstem slices (n = 11). D) LDH-activity assay from brainstem slices, treated as described above. In the eluate, a low and constant LDH activity was observed throughout, treatment with capsaicin did not alter LDH activity. Triton-X 100 employed as a positive control increased LDH activity in all samples (*); there was no difference between the brainstem slices previously treated with capsaicin 100 nM (filled symbols) and those without (open symbols, n = 4 each). No increase in LDH activity was observed 1, 2, 4 and 8 h after preparation (n = 3, not shown). Data are mean ± SEM.