Fig. 3

Jejunal motility in response to EA at LI11 under the administration of the sympathetic pathway. Aa Representative tracings of jejunal motility regulated by EA without and with the administration of propranolol and clenbuterol in rats. Ab Compared with the jejunal pressure before EA, changes were observed during EA in the control group, propranolol group and clenbuterol group. Propranolol promoted jejunal pressure significantly and clenbuterol led to the opposite effect, whereas EA at LI11 increased jejunal pressure in all three groups, which had statistical significance. Data are expressed as mean ± SEM (n = 8 rats per group at each time period). ^* P < 0.05 vs pre-EA, paired t-test. Ac Promotion percentages of jejunal pressure by EA in three rat groups are shown, and each change rate was above 105%. The promotion rate of EA was not significantly different among the groups. ^# P > 0.05 vs each group, One-way ANOVA. Data are expressed as mean ± SEM (n = 8 rats and mice). Ba Representative tracings of jejunal motility regulated by EA in WT mice and β₁β₂ ^−/−mice. Bb Compared with the jejunal pressure before EA at the same intensity, changes were observed during EA in both the WT and β₁β₂ ^−/− groups. Thus, EA at LI11 increased jejunal pressure of both groups of mice significantly. Data are expressed as mean ± SEM (n = 8 mice per group at each time period). ^Δ P < 0.05 vs pre-EA, paired t-test. Bc Promotion percentages of jejunal pressure by EA in two mouse groups are shown, and each change rate was above 105%. The promotion rate of EA was not significantly different among the groups. ^# P > 0.05 vs each group, One-way ANOVA. Data are expressed as mean ± SEM (n = 8 rats and mice). EA, electroacupuncture; prop, propranolol; clen, clenbuterol. WT, wild-type