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The cerebellar cortex contains at least two classes of Purkinje cells, which are organized into alternating arrays of parasagittal bands. The clearest demonstration of this compartmentation is the pattern of expression of a family of polypeptide antigens, the zebrins, which are expressed selectively by Purkinje cell subsets. Furthermore, anterograde tracing experiments show that the zebrin compartments are closely correlated with both afferent and efferent projection maps. The further subdivision of long parasagittal bands into smaller modules may occur through several different mechanisms, including the intrinsic cerebellar lobulation and the selective distribution of afferent terminal fields. However, while the longitudinal subdivisions are straightforwardly shown, the mediolateral boundaries are more subtle. In this report we describe a novel mediolateral and anteroposterior compartmentation boundary in mice, running across lobule VIII, that is revealed by the consequences of the lurcher (Lc/+) allele for zebrin expression. In normal mice zebrin compartmentation develops in several discrete stages: until postnatal day 5 (PD5) there is no zebrin expression; from PD5-PD7 zebrin is found only in the posterior lobe vermis, with immunoreactive Purkinje cells in lobules X, IX, and VIII but not elsewhere; from PD7-PD12 most Purkinje cells in the vermis become zebrin+; from PD12-PD15 immunoreactivity also appears in the hemispheres so that almost all Purkinje cells now are zebrin+; and finally, from PD15-PD25 zebrin is gradually suppressed in those Purkinje cells that are zebrin- in the adult until the mature pattern of parasagittal compartments is revealed. In the Lc/+ mutant the normal developmental progression is interrupted at around PD7. As a result, the pattern of zebrin expression becomes frozen at that stage when immunoreactive Purkinje cells are confined exclusively to the posterior lobe vermis. A reproducible boundary between expressing and nonexpressing zones runs mediolaterally across the dorsal surface of lobule VIII. Apart from zebrin expression itself, there are no obvious structural correlates of this transition. This mediolateral boundary identifies a developmental unit in the posterior lobe vermis of the cerebellum, and provides further evidence that the cerebellum is a highly heterogeneous structure.

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Previous studies in our laboratory have shown that cortical lesions induced by thermocoagulation of pial blood vessels, but not by acute aspiration, result in 1) the preservation of control levels of the growth-associated protein (GAP)-43 and 2) a prolonged increase in neurotransmitter gene expression in the denervated dorsolateral striatum. We have examined whether corticostriatal projections from the spared homotypic contralateral cortex contribute to these effects. Adult rats received either a thermocoagulatory or aspiration lesion of the cerebral cortex and, after 30 days, received an injection of the anterograde tracer, Fluoro-Ruby, in the contralateral homotypic cortex. Rats were killed 7 days later, and labeled fibers were examined with fluorescence microscopy in the ipsilateral and contralateral striata. Ipsilateral corticostriatal projections were detected in lesioned and unlesioned rats. Numerous labeled fibers were detected in the contralateral striatum of thermocoagulatory-lesioned but not aspiration-lesioned or control animals, suggesting that contralateral cortical neurons may undergo axonal sprouting in the denervated striatum following a thermocoagulatory lesion of the cortex. To determine whether contralateral corticostriatal fibers play a role in the changes in striatal gene expression induced by the thermocoagulatory lesions, the effects of aspiration lesions, as well as unilateral and bilateral thermocoagulatory lesions of the cortex were compared. Confirming previous results, striatal enkephalin mRNA levels were increased after a unilateral thermocoagulatory lesion. However, they were unchanged after aspiration or bilateral thermocoagulatory lesions, suggesting that sprouting or overactivity of contralateral corticostriatal input contributes to the increase seen after unilateral thermocoagulatory lesions.