G protein-coupled receptors are the largest receptor family in humans and are involved in the regulation of many physiologically important functions. Thus, many drugs target these receptors. Nanoparticles (NPs) which have gained massive attention in the biomedical field during the last years can be functionalized with ligands of G protein-coupled receptors. Compared to “classical” single molecules, nanoparticles which are functionalized with these molecules can improve their efficacy, transport them over biological barriers and may reduce their side effects. For my project, gold nanoparticles were functionalized with carbachol, adrenaline, noradrenaline and additionally with the muscarinic receptor antagonist atropine. The aim of my project was to find out whether biofunctionalized gold NPs are effective at adrenergic or cholinergic receptors in pharmacologically interesting tissues. Adrenaline functionalized NPs induced a K+ secretion at the distal colon, which expresses several subtypes of ? adrenoceptors. Contractility studies with isolated cardiomyocytes revealed that the adrenergic NPs enhance the inotropy of cardiac muscle cells by stimulating ?1 receptors (which was inhibited by the ?1 specific antagonist atenolol). Muscular ?2 receptors, which are targeted to relax the airways in obstructive lung diseases, are not stimulated by adrenaline or noradrenaline functionalized gold NPs. In contrast, atropine-functionalized NPs could relax respiratory smooth muscle cells in subnanomolar concentrations. For a possible oral application of the NPs, the bioavailability after oral administration is very important. Thus, atropine-functionalized NPs were applied at the mucosal side of the jejunum and I investigated whether they can inhibit muscarinic receptors on the basolateral side of epithelial cells or on smooth muscle cells of the tunica muscularis. Indeed, the atropine-NPs did reduce the intestinal Cl- secretion induced by the stable acetylcholine derivative carbachol as well as contractions which were evoked by electric stimulation of cholinergic neurons of the enteric nervous system. Both, the intestinal Cl- secretion and contractions were inhibited in a time-dependent manner suggesting delayed passage of the NPs across the intestinal epithelium. Atropine-functionalized NPs were synthesized with diameters between 8 and 16 nm in 1 to 2 nm size steps. I found out that 12 to 14 nm sized NPs were most effective to inhibit the carbachol-induced Cl--secretion, while smaller or larger NPs were less effective. Transmission electron microscope images revealed that NPs can be internalized into cells via endocytosis, suggesting that the NPs crossed the intestinal epithelium through transcytosis. A massive potentiation, i.e. an increase of the affinity towards the receptors was observed for carbachol-functionalized gold nanoparticles in previous studies of my work group. In my experiments, picomolar concentrations of carbachol-functionalized gold nanoparticles led to an increase of isometric muscle force of intestinal smooth muscle segments and a rise of the cytosolic Ca2+ concentration. This increase of the cytosolic Ca2+ concentration was more stable compared to the one stimulated by native carbachol. The results of my project show that cholinergic and adrenergic functionalized gold nanoparticles can bind to their respective G protein-coupled receptors (except for ?2 receptors). These receptor interactions are dependent on the diameter of the gold NPs. Moreover, the NPs cross the intestinal epithelium in a time-dependent manner. Therefore, the biofunctionalized NPs are suitable candidates for further studies to investigate whether they could be used as a treatment for gastrointestinal or respiratory diseases.