The real-time observation of cell nents of Ca 2/ fluctuations in the somata of migrating movement in acute cerebellar slices reveals that grangranule cells. Interestingly, each phase of Ca 2/ flucule cells alter their shape concomitantly with changes tuation controls a separate phase of saltatory movein the mode and rate of migration as they traverse ment in the granule cells: The cells move forward different cortical layers. Although the origin of local during the phase of transient Ca 2/ elevation and reenvironmental cues responsible for these position-spemain stationary during the troughs. Consequently, the cific changes in migratory behavior remains unclear, changes in the amplitude and frequency components several signaling mechanisms involved in controlling of Ca 2/ fluctuations directly affect granule cell movegranule cell movement have emerged. The onset of ment: Reducing the amplitude or frequency of Ca 2/ one such mechanism is marked by the expression of fluctuations slows down the speed of cell movement, voltage-gated ion channels and neurotransmitter rewhile the enhancement of these components accelerceptors in postmitotic cells prior to the initiation of ates migration. These findings suggest that signaling their migration. Granule cells start their radial migramolecules present in the local cellular milieu encountion after the expression of N-type Ca 2/ channels and tered on the migratory route control the shape and the N-methyl-D-aspartate subtype of glutamate recepmotility of granule cells by modifying Ca 2/ fluctuators on the plasmalemmal surface. Blockade of the tions in the soma through the activation of specific ion channel or receptor activity significantly decreases the channels and neurotransmitter receptors. α§ 1998 John rate of cell movement, indicating that the activation