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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Brain Behav Immun. 2019 Aug 22;82:214–223. doi: 10.1016/j.bbi.2019.08.188

Fig 3. Optogenetic stimulation of sympathetic neurons in the SMG induces β2AR dependent Ach release in MLN and spleen.

Fig 3.

Stimulation of sympathetic neurons expressing ChR2 in the SMG induces the release of NE in the MLN (A, left panel) and spleen (B left panel) of mice treated with vehicle (blue bars) or the highly selective β2AR antagonist ICI 118 551 (red bars). While stimulation evokes ACh release in the MLN and spleen of vehicle treated mice (blue bars), no increase in ACh is detected in the animals treated with ICI 118 551 (red bars, A & B, right panel). In a separate cohort of animals, we compared NE and ACh released before (baseline) and after i.v. injection of vehicle or ICI 118 551 (C). n= 6–10 mice per group in 3 experiments, †P<0.05 between indicated groups, #,* P <0.05, between all other groups, ANOVA Tukey post-test, data are presented as mean ± SEM for all panels.