a, Raw population bursts from PiCo and contralateral
preBötC with the progressive addition of 1 μM mecamylamine
(nicotinic receptor antagonist), 10 μM atropine (muscarinic receptor
antagonist), and 4 μM norepinephrine. b, The left two
graphs show n=5 experiments in which atropine was applied first, and
the right graphs illustrate n=3 experiments in which mecamylamine
was applied first. Blockade of muscarinic receptors results in a larger
decrease in PiCo burst frequency than blocking nicotinic receptors, while
preBötC frequency does not change significantly (top graphs).
Interestingly, blockade of muscarinic receptors increases the amplitude of
PiCo bursts (bottom graphs). The PiCo rhythm persists after concurrent
blockade of both types of acetylcholine receptors, and PiCo burst frequency
rebounds to near baseline levels when an additional 2 μM NE is
applied (total 4 μM NE; top graphs). (mean ± s.e.m.).
Two-way ANOVA followed by a Bonferroni post hoc test.
**P < 0.01,
*P < 0.05 comparing preBötC to PiCo,
ϕ P<0.05 compared to baseline (2 μM
NE).