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Acetylcholine (ACh) is an important neurochemical transmitter in animals; it also exists in plants and plays a significant role in various kinds of physiological functions in plants. ACh has been known to induce the stomatal opening. By monitoring the changes of cytosolic Ca2+ with fluorescent probe Fluo-3 AM under the confocal microscopy, we found that exogenous ACh increased cytosolic Ca2+ concentration of guard cells ofVicia faba L. Muscarine, an agonist of muscarine acetylcholine receptor (mAChR), could do so as well. In contrast, atropine, the antagonist of mAChR abolished the ability of ACh to increase Ca2+ in guard cells. This mechanism is similar to mAChR in animals. When EGTA was used to chelate Ca2+ or ruthenium red to block Ca2+ released from vacuole respectively, the results showed that the increased cytosolic Ca2+ mainly come from intracellular Ca2+ store. The evidence supports that Ca2+ is involved in guard-cell response to ACh and that Ca2+ signal is coupled to mAChRs in ACh signal transduction in guard cells. [ABSTRACT FROM AUTHOR]

Acetylcholine (ACh) is an important neurochemical transmitter in animals; it also exists in plants and plays a significant role in various kinds of physiological functions in plants. ACh has been known to induce the stomatal opening. By monitoring the changes of cytosolic Ca2+ with fluorescent probe Fluo-3 AM under the confocal microscopy, we found that exogenous ACh increased cytosolic Ca2+ concentration of guard cells of Vicia faba L. Muscarine, an agonist of muscarine acetylcholine receptor (mAChR), could do so as well. In contrast, atropine, the antagonist of mAChR abolished the ability of ACh to increase Ca2+ in guard cells. This mechanism is similar to mAChR in animals. When EGTA was used to chelate Ca2+ or ruthenium red to block Ca2+ released from vacuole respectively, the results showed that the increased cytosolic Ca2+ mainly come from intracellular Ca2+ store. The evidence supports that Ca2+ is involved in guard-cell response to ACh and that Ca2+ signal is coupled to mAChRs in ACh signal transduction in guard cells. [ABSTRACT FROM AUTHOR]

Investigates the role of acetylcholine (Ach) on plant root-shoot communication using the root-split system of Vicia faba L. Decrease of Ach content in root tips and increase in the xylem sap transported per time unit, due to a slight osmotic stress; Probable function of Ach content decrease to regulate stomatal behavior.

Proposes a model for the osmoregulation in guard cell vacuoles (GCV) for stomatal opening. Disaggregation of some polymerized particles inside GCV; Process of osmoregulation that avoids the massive energy consuming transportation across cell membranes, which is a foundation of the chemosmotic hypothesis.

Studies the effects and the relationship between salicylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement. Evidence that exogenous SA and NO induced stomatal closure; Suggestion that both cGMP and cADPR might mediate the signal transduction of SA and NO-based stomatal closure.

Discusses the involvement of Ca2+/CaM in the signal transduction of acetylcholine regulating stomatal movement. How the neutrotransmitter acetylcholine (ACh) is able to regulate the movement of stomata in plants; Demonstration that Ca2+/CaM are also involved in the ACh regulated stomatal movement.

Features a study that used the fluorescent BODIPY FL-labeled 3-2'-aminobenzhydryloxy tropane to detect muscarinic acetylcholine receptors (mAChR) in plant guard cells. Localization of mAChR in the abaxial epidermis of Vicia faba L; Distribution of mAChR in the guard cell protoplasts of Vicia faba L; Localization of mAChR in the abaxial dermis of Pisum sativum L.

The inward rectified potassium current of Vicia faba guard cell protoplasts treated with acetylcholine (ACh) or the antagonists of its receptors were recorded by employing the patch clamp technique. The results show that ACh at lower concentrations increases the inward K+ current, in contrast, ACh at higher concentrations inhibits it. Treated with d-Tubocurarine (d-Tub), an antagonist of the nicotine ACh receptor (nAChR) inhibits the inward K+ current by 30%. Treated with atropine (Atr), an antagonist of the muscarine (Mus) ACh receptor (mAChR) also inhibits it by 36%. However, if guard cell protoplasts are treated with d-Tub and Atr together, the inward K+ current is inhibited by 60% –75%. Tetraethylammonium chloride (TEA), a strong inhibitor of K+ channels has no effect on the inward K+ current regulated by ACh, suggesting that there are inward K+ channels modulated by AChRs on the membrane of the guard cell protoplasts. These data demonstrate an ACh-regulated mechanism for stomatal movement. [ABSTRACT FROM AUTHOR]

In animal cells, actions of acetylcholine depend on its binding to specific receptors. Activation of nicotinic acetylcholine receptor can affect the membrane permeability to ions directly. As concerned about acetylcholine regulating stomatal movement, nicotinic acetylcholine receptor may also be involved. Experiments with nicotinic acetylcholine receptor antagonist (D-tubocurarine) and agonist (nicotine) showed that nicotinic acetylcholine receptor was involved in acetylcholine inducing stomata1 opening. In addition, these 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 containing Ca2+, The result by Western blotting showed that at least α-and β-subunits of nicotinic receptor existed in microsomes of guard cell protoplasts. It was found that the distribution of nicotinic acetylcholine receptor was mainly on the surface of protoplasts as shown by FITC labelled α-bungarotoxin. The results above show that nicotinic acetylcholine receptor exists in guard cells and mediates acetylchlone to induce stomatal opening. [ABSTRACT FROM AUTHOR]

Provides information on a study which showed that agonists of muscarinic receptor could induce stomatal opening, while the antagonists could block stomatal opening induced by acetylcholine. Materials and methods; Results and discussion.

Examines the effects of microfilament and microtubule inhibitors and periodic electrical impulses on phloem transport in pea seedling. Amount of sap transported from source to sink measured by increase in root elongation; Phloem translocation of assimilates in higher plant.