Fig. 3: Lithium prevents demyelination and axon shortening in peripheral nerve fibers of animals treated with MMAE.
From: Chemotherapy-induced neuropathy in monomethyl Auristatin E treatment: prevention by lithium

a Representative images from ex vivo DRG proximal nerve fibers stained with FM1-43 showed reduction in myelin width in the MMAE group and its prevention in LiCl+MMAE group. White arrows indicate nodes of Ranvier and red traces represent the myelin width, which was measured and quantified in panel 4D. Scale bar 20 μm. b Representative images of CARS imaging of sciatic nerve fibers, indicating a similar reduction in myelin width in the group treated with MMAE and its prevention by LiCl coadministration. White arrows indicate nodes of Ranvier and yellow traces represent the myelin width, which was measured and quantified in panel 4E Scale bar 20 μm. c Representative images of immunohistochemistry of IENF with TUJ1 antibody, showing a reduction in the number of neuronal terminations in the paw of animals treated with MMAE, which was prevented by lithium treatment. White arrows indicate intraepidermal neuronal terminations. d Quantification of the diameter of the ex vivo DRG axons showed reduction in myelin diameter in the MMAE group compared to the saline or lithium groups (p < 0.0001, n = 3 animals each group). Lithium administration was able to prevent the reduction, with myelin width comparable to the control (p > 0.05). e Quantification of the myelin diameter in sciatic nerves presented a reduction in the MMAE group compared with saline (p < 0.0001, n = 3 animals each group), and its prevention by lithium (p > 0.05 compared to saline). f Quantification of IENF shows a lower number of neuronal terminations in the paw of MMAE treated animals (p < 0.05, n = 3 animals each group) and its prevention when lithium is used in coadministration (p > 0.05 compared to saline).