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Trafficking of secretory vesicles along neurites of PC12 cells was visualized by 2D and 3D real-time imaging using fluorescence microscopy. Vesicle motion along distinct pathways was directly seen. From an overlay of individual pathways, the underlying cytoskeletal filament could be imaged at a subwavelength resolution. Continuous vesicle transport was interrupted by periods of diffusive motion with concomitant pathway changes. Statistical analysis shows that such interruptions were distributed stochastically along the filament, indicating a limited processivity of motor proteins also in a cellular context. Periods of diffusive motion facilitated the interaction with actively transported vesicles. Frequent associations and dissociations of vesicles have been observed consistently, pointing to a functional relevance of vesicle cotransport. Microsc. Res. Tech. 63:159–167, 2004. © 2004 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The present study revealed the localization of neuronal calcium sensor (NCS)-1 immunoreactivity (IR) in the developing rat spinal cord. The NCS-1 IR first appeared at embryonic day 12 in the peripheral nerves and their somata. Intense NCS-1 IR was expressed in ascending and descending tracts in the white matter during the late prenatal period, which gradually decreased to the faint level during postnatal development. Intense NCS-1 IR was colocalized with growth associated protein (GAP)-43 IR in the marginal zone and with the glutamate-aspartate transporter (GLAST) IR in the radial processes traversing the marginal zone. In the adult rat white matter, radially oriented astrocytes and astrocytes in the glia limitans were double-labeled for NCS-1 and glial fibrillary acidic protein (GFAP), whereas small dots on finger-like dendritic projections were double-labeled for NCS-1 and synaptophysin. In the developing gray matter, the NCS-1 IR appeared at embryonic day 12 and gradually increased in the neuronal somata and neuropil, reaching a plateau after the end of the 4th postnatal week. The small dots in neuropil were colabeled for NCS-1 and GFAP or NCS-1 and synaptophysin in the adult rat gray matter. These results strongly suggest that NCS-1 is involved in axogenesis and synaptogenesis in the developing rat spinal cord. NCS-1 can serve as a Ca2+-sensor not only in neurons but also in radial glial cells or even in radially oriented astrocytes in the adult rat spinal cord. J. Comp. Neurol. 460:465–475, 2003. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Neuronal calcium sensor-1 (NCS-1) is a member of the EF-hand calcium-binding protein superfamily, which is considered to modulate synaptic transmission and plasticity. The detailed distribution of NCS-1 was analyzed in the mouse cerebellar cortex. In coronal sections, the NCS-1 immunostaining displayed characteristic parasagittal banding pattern in the Purkinje cell layer and molecular layer, while there were no apparent bands in the granule cell layer. The alternating positively and negatively NCS-1–labeled Purkinje cell clusters contributed to this cerebellar compartmentation. In contrast, stellate-basket cells were uniformly NCS-1–positive throughout the cerebellum. Immunofluorescent double staining showed that NCS-1 and zebrin II exhibited a similar parasagittal banding pattern. Then, we performed mapping of NCS-1– and/or zebrin II–labeled Purkinje cell somata using seven sequential coronal sections. NCS-1–positive/zebrin II–positive Purkinje cell clusters were seen throughout the cerebellum, but NCS-1–positive/zebrin II–negative Purkinje cells were exceedingly rare. On the other hand, NCS-1–negative/zebrin II–positive Purkinje cell clusters were found in anterior lobule vermis and paraflocculus, whereas they were rarely seen in posterior lobules. The digitized quantitative analysis showed close relationship between NCS-1 and zebrin II immunoreactivity in the molecular layer. The correspondence between NCS-1 and zebrin II demonstrated here indicates a novel anteroposterior difference of cerebellar compartmentation and provides fundamental information of cerebellar organization. J. Comp. Neurol. 458:412–424, 2003. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]