No abstract

The distribution of spinocerebellar projections from birth to adulthood in rats was analyzed by anterograde and retrograde tracing methods. A correlation between mossy fiber synaptogenesis and the establishment of spinocerebellar topography was also investigated with electron microscopy. Experiments with retrograde transport techniques indicate that the spinal axons reach the cerebellum in two successive groups: the first one, appearing prenatally, contains axons from neurons in the central cervical nucleus, Clarke's column, the sacral nucleus of Stilling, as well as from border cells. The second group, which reaches the cerebellum by P3, arises from new neurons of the same nuclear regions and from scattered cells of the spinal gray matter. The distribution and the morphological appearance of the spinal cells change between P1 and P3 and give the adult pattern by P7. The establishment of spinocerebellar projections occurs in four successive stages. In a first stage, spinal axons reach the cerebellum and occupy the prospective white matter of the anterior vermal lobe and of the pyramis. Later, during a "waiting" stage between P1 and P3, the spinal fibers become denser in the central white matter of both their anterior and posterior target zones but do not penetrate the gray matter. From P3 to P5 the protocolumnar stage takes place, and spinal axons invade the granular layer of the anterior lobe, where they begin to be organized in nascent sagittal columns. At the end of this stage, identifiable synaptic contacts between mossy terminals and granule cell dendrites are first observed in the anterior lobe by electron microscopy. In the pyramis, invasion of the granular layer begins only at P5. Between P5 and P7 the low intercolumnar dispersion of spinal fibers disappears and the projection reaches its fourth and final stage, characterized by a columnar organization corresponding to the adult pattern of the spinocerebellar projection. These results indicate that (1) the adult pattern of spinocerebellar projections is attained by P7. (2) The asynchronous invasion of the gray matter in the anterior and posterior lobes may be related to the chronology of mossy fiber maturation in these regions. (3) There is a temporal correlation between the columnar organization of the spinal axons and the appearance of the earliest-maturing mossy rosettes. However, a clear relationship between synaptogenesis and topographic organization could not be demonstrated.

Letters to the Editor 901 RCP mutations reported by Nathans et al. (1989) to cause reduced visual acuity but with normal fundus. In fact, figure 2 in the article by Nathans et al. (1989) shows a fundus photograph from a patient with "progressive bilateral central retinal degeneration" (p. 832). Other patients are described as having macular lesions and atrophy, on ophthalmic examination. Therefore, a phenotype such as the one Bergen and Pinckers observed in this family evidently could result from a mutation or combination of mutations in the red-and green-pigment genes. In these circumstances, exclusion of these genes is essential before a new locus is assigned.Bergen and Pinckers do indeed describe a multipoint analysis using markers DXS8103 and DXS8069, apparently spanning the RCP and GCP genes, that excludes these genes. However, this evidence is given as "data not shown," no LOD scores for these markers are included in table 3, and no reference is given to a published map proving that these markers span the genes in question. Furthermore, the authors' assertion that "Southern blot analysis with an RCP/GCP cDNA probe)did not reveal any structural abnormalities" (Bergen and Pinckers 1997, p. 1,472) surely is insufficient, since abnormalities at this locus can result from point mutations or from rearrangements 4-kb upstream of the red cone-pigment gene and 43-kb upstream of the green cone-pigment gene. Therefore, although data excluding the RCP/GCP locus in this family may exist, this could not be proved on the basis of the results presented.

No abstract