The effect of water-soluble pristine C₆₀ fullerene nanoparticles (C₆₀NPs) on receptor-operated cation channels formed by TRPC4/C6 proteins in ileal smooth muscle cells was investigated for the first time. Activation of these channels subsequent to acetylcholine binding to the expressed in these cells M₂ and M₃ muscarinic receptors represents the key event in the parasympathetic control of gastrointestinal smooth muscle motility and cholinergic excitation-contraction coupling. Experiments were performed on single collagenase-dispersed mouse ileal myocytes using patch-clamp techniques with symmetrical 125 mM Cs⁺ solutions and [Ca^2 +]_i ‘clamped’ at 100 nM in order to isolate the muscarinic cation current (mI_CAT). The current was induced by intracellular infusion of 200 μM GTPγS, which activates G-proteins directly, i.e. bypassing the muscarinic receptors. C₆₀NPs applied at 10^− 6 M at peak response to activation of G-proteins caused mI_CAT inhibition by 47.0 ± 3.5% (n = 9). The inhibition developed rather slowly, with the time constant of 119 ± 16 s, was voltage-independent and irreversible. Thus, C₆₀NPs are unlikely to cause any direct block of TRPC4/C6 channels; rather, they may accumulate in the membrane and disrupt G-protein signalling leading to mI_CAT generation. C₆₀NPs may represent a novel class of biocompatible molecules for the treatment of disorders associated with enhanced gastrointestinal motility.

首次研究了水溶性原始C ₆₀富勒烯纳米颗粒（C ₆₀ NPs）对回肠平滑肌细胞中TRPC4 / C6蛋白形成的受体操纵的阳离子通道的影响。这些通道在乙酰胆碱结合到这些细胞M ₂和M ₃毒蕈碱受体中表达后的激活代表了胃肠道平滑肌运动副交感控制和胆碱能兴奋-收缩偶联中的关键事件。使用膜片钳技术在对称的125 mM Cs ⁺溶液和[Ca ^{2 +} ] _i上对单个胶原酶分散的小鼠回肠心肌细胞进行了实验“钳位”在100 nM，以分离毒蕈碱阳离子电流（mI _CAT）。该电流是由200μMGTPγS的细胞内输注引起的，它直接激活G蛋白，即绕过毒蕈碱受体。在 对G蛋白活化达到峰值的情况下，以10 ^-6 M的浓度施用C ₆₀ NP引起的mI _CAT抑制为47.0±3.5％（n = 9）。抑制作用发展缓慢，时间常数为119±16 s，与电压无关且不可逆。因此，C ₆₀ NP不太可能引起TRPC4 / C6通道的任何直接阻塞。相反，它们可能积聚在膜中并破坏G蛋白信号传导，从而导致mI _CAT生成。C ₆₀NP可代表一类新型的生物相容性分子，用于治疗与胃肠动力增强相关的疾病。