In animal cells, actions of acetylcholine depend on its binding to specific
receptors. Activation of nicotinic acetylcholine receptor can affect the m
embrane permeability to ions directly. As concerned about acetylcholine reg
ulating stomatal movement, nicotinic acetylcholine receptor may also be inv
olved. Experiments with nicotinic acetylcholine receptor antagonist (D-tubo
curarine) and agonist (nicotine) showed that nicotinic acetylcholine recept
or was involved in acetylcholine inducing stomatal opening. In addition, th
ese effects of D-tubocurarine and nicotine on stomatal movement can only be
found in medium containing K+ while no effects can be found in medium cont
aining Ca2+. The result by Western blotting showed that at least alpha- and
beta-subunits of nicotinic receptor existed in microsomes of guard cell pr
otoplasts. It was found that the distribution of nicotinic acetylcholine re
ceptor was mainly on the surface of protoplasts as shown by FITC labelled a
lpha-bungarotoxin. The results above show that nicotinic acetylcholine rece
ptor exists in guard cells and mediates acetylchlone to induce stomatal ope
ning.