Transverse boundaries divide the cerebellar cortex into four transverse zones, and within each zone the cortex is further subdivided into a symmetrical array of parasagittal stripes. Several molecules believed to mediate long-term depression at the parallel fiber-Purkinje cell synapse are known to be expressed in stripes. We have therefore explored the distributions of phospholipase Cbeta3 and phospholipase Cbeta4, key components in the transduction of type 1 metabotropic glutamate receptor-mediated responses. The data reveal that both phospholipase Cbeta isotypes are expressed strongly in the mouse cerebellum in subsets of Purkinje cells. The two distributions are distinct and largely nonoverlapping. The pattern of phospholipase Cbeta3 expression is unique, revealing stripes in three of the four transverse zones and a uniform distribution in the fourth. In contrast, phospholipase Cbeta4 appears to be confined largely to the Purkinje cells that are phospholipase Cbeta3-negative. PLCbeta3 is restricted to the zebrin II-immunopositive Purkinje cell subset. Not all zebrin II-immunoreactive Purkinje cells express PLCbeta3: in lobules IX and X it is restricted to that zebrin II-immunopositive subset that also expresses the small heat shock protein HSP25. PLCbeta4 expression is restricted to, and coextensive with, the zebrin II-immunonegative Purkinje cell subset. These nonoverlapping expression patterns suggest that long-term depression may be manifested differently between cerebellar modules.

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Niemann Pick disease type C1 (NPC1) is an inherited, autosomal recessive, lipid-storage disorder with major neurological involvement. Purkinje cell death is a prominent feature of the neuropathology of NPC. We have investigated Purkinje cell death in two murine models of NPC1, BALB/c npc(nih) and C57BLKS/J spm. In both cases, extensive Purkinje cell death was found in the cerebellum. The pattern of Purkinje cell death is complex. First, zebrin II-negative Purkinje cells disappear, to leave survivors aligned in stripes that closely resemble the pattern revealed by using zebrin II immunocytochemistry. Subsequently, as the disease progresses, additional Purkinje cells die. At the terminal stages of the disease, the surviving Purkinje cells are concentrated in lobules IX and X of the posterior lobe vermis. Purkinje cell degeneration is accompanied by the ectopic expression of tyrosine hydroxylase and the small heat shock protein HSP25, both associated preferentially with the surviving cells. The pattern of cell death thus reflects the fundamental compartmentation of the cerebellum into zones and stripes.

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Group-housed laboratory mice are frequently found with their whiskers and facial hair removed. It has been proposed that dominant mice are responsible for barbering the hair of the recipient (the Dalila effect), and early studies suggest that the hair is removed by nibbling. In the present study, pairs of C57BL6 mice, composed of a barber and recipient, were separated to allow hair to regrow. The animals were then placed together in an observation box and their social behavior was videorecorded. The videorecording was subjected to frame-by-frame analysis. Barbering was found to occur during acts of mutual grooming. During grooming, one member of a mouse pair removed the vibrissae of the conspecific and did so by grasping individual whiskers with the incisors and plucking them out. Although plucking appeared 'painful', recipients were passive in accepting barbering, and even pursued conspecifics for further grooming. Other measures indicated that barbers were heavier than recipients and brain weights were not different. Although cortical barrel fields appeared normal to cytochrome oxidization and zinc staining, Golgi analysis of layer three, barrel-field basilar dendrites indicated changes in cell morphology. The results are discussed in relation to the hypothesis that barbering is an expression of social dominance, the origins of the barbering behavior, and the consequences of barbering on brain function.