Developing Central Nervous System and Vulnerability to Platinum Compounds

Figure 4

Purkinje cell differentiation and synaptogenesis: GAD67 immunoreaction. Treatment with dose of 5 μg/g b.w. At PD11 (a)–(d), in control rats (a), GAD67 labelling is shown in the entire Purkinje neurons and the dot-like nerve terminals in the ML, and the inhibitory components (Golgi neuron axons) of the glomeruli in the IGL. After cisPt treatment, a marked delay in the Purkinje cell dendrite growth and a low number of punctuate nerve terminals in the ML are observed (b). The GAD67 labelling after PtAcacDMS displays almost normal patterns (c), except for presence of axonal swellings in the form of spheroids in some Purkinje cells (d, arrow). At PD17 (g, h), seven days after treatments, differently from cisPt (not shown), the GAD67 immunopositive baskets at the Purkinje cell axon hillock (arrows) are apparently normal (as in controls, g) after PtAcacDMS at low dose (h). Treatment with dose of 10 μg/g b.w. At PD11 (e, f), the Purkinje cell differentiation is further delayed after cisPt (e), differently from that observed in PtAcacDMS rats (f). At PD17 (i, j), deeply altered baskets and lack of immunopositive nerve terminals in the ML are observed after cisPt (i); the treatment with PtAcacDMS induces several recurrent collaterals of ganglionic plexuses in some tracts of convolutions, but dot-like immunopositive terminals are present in the ML (j). Magnification: 40x.

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