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. Author manuscript; available in PMC: 2010 Aug 3.
Published in final edited form as: Eur J Neurosci. 2003 Nov;18(9):2515–2526. doi: 10.1046/j.1460-9568.2003.02935.x

Fig. 3.

Fig. 3

(A) Potentiation of capsaicin-evoked immunoreactive calcitonin gene-related peptide (iCGRP) release by cytisine. Tissue was washed for 70 min with physiologic Krebs buffer (pH 7.4), followed by a 10-min superfusion of separate groups with capsaicin alone (100 μM, n = 6) or capsaicin plus cytisine (1 nM–1 μM, n = 5–6/group). Data are expressed as percentage control of net peak iCGRP release, calculated as the arithmetic difference between peak and basal release in fmol/sample. Concentration required to produce 50% effect (EC50) was 4.831 nM and maximal effect (Emax) was 76.2% over control. (B) Reversal of potentiation by cytisine of capsaicin-evoked iCGRP release by mecamylamine. Mecamylamine (10 μM) was given 20 min before, 10 min during and 10 min following 1 μM cytisine + capsaicin superfusion. Groups were analysed by an unpaired, one-tailed Student’s t-test (*P < 0.05) and data are represented as mean ±SEM.