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. 2003 May 1;23(9):3669–3678. doi: 10.1523/JNEUROSCI.23-09-03669.2003

Fig. 5.

Fig. 5.

Effect of inhibiting connexon delivery to the plasma membrane on the increase in gap junctional coupling in hexamethonium-treated slices. Connexon trafficking from the Golgi apparatus to the plasma membrane was abolished by treating slices with either BFA (2 μg/ml) or the cytoskeletal disrupting agent nocodazole (25 μm) for at least 30 min before adding 200 μm hexamethonium. A, a, Immunofluorescent labeling of the TGN using an antibody directed against TGN38. As expected, the labeling appeared as a fluorescent crescent near the nucleus (inset: scale bar, 5 μm) in untreated slices, whereas the Golgi network was dramatically disorganized in BFA-treated slices.A, b, Microtubules were immunolabeled with an antibody directed against β-tubulin. Nocodazole treatment strongly disrupted the cytoskeleton, as seen by the absence of β-tubulin detection.B, Pooled data showing that treatment with either BFA or nocodazole abolished the increase in LY spreading in hexamethonium-containing medium. *p < 0.01 compared with control.