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Cerebellar Development
in the Mouse: Genetics, Cell Biology, and Gene Expression
Our research is aimed at understanding cell-cell
interactions leading to neuronal differentiation and synaptogenesis. We
focus on the interrelated processes of afferent growth and dendrite and
spine development in target neurons of the CNS. The cerebellum is an attractive
model system for exploring these issues . It has a limited number of cell
types, many cell type-specific markers, and a regular architecture and
wiring pattern. Degeneration of Purkinje cells, the main output neurons
of the cerebellum, occurs in many neurological diseases and in known mutant
mouse strains. The cerebellum undergoes extensive development postnatally
in rodents, providing a readily accessible experimental setting for studying
neuronal migration, differentiation, and synaptogenesis. We are exploring
these processes using the tools of genetics, genomics, and cell biology.
Genetic approaches: We are taking part in
a genetic screen for new mouse mutants with abnormal cerebellar development.
As part of a collaboration with the Genomics Institute of the Novartis
Research Foundation, we will have access to several new mouse strains
that may be used as models for understanding human cerebellar ataxias.
To date, 5 such strains have been identified. One strain has been mapped,
a second strain is being mapped, and three other probands are being bred
in preparation for mapping as of this report.
Genomic approaches: We are conducting expression
profiling for the developing cerebellum using Affymetrix gene chips. We
are comparing the levels of gene expression in cerebella from early postnatal
wild type mice with those from several strains of known cerebellar mutant
mice, in an attempt to reveal novel gene expression pathways that are
altered when cerebellar development is abnormal. In this way, we hope
to gain insight into the signaling pathways necessary for normal cerebellar
development, and possible targets for intervention in cases of cerebellar
ataxia.
Cell biology approaches: We are using primary
neuron cultures to explore the cell-cell interactions necessary for granule
and Purkinje cell development. Purified Purkinje cells survive and produce
an axon, but no mature dendrite. Adding back the cerebellar granule cells,
afferents for the Purkinje cells, triggers the development of dendrites
and spines on the Purkinje cells, recapitulating the steps of differentiation
seen in vivo. This culture system allows us to test inhibitors and stimulators
of specific signal transduction pathways for their effects on cerebellar
granule and Purkinje cells. We are pursuing preliminary data indicating
that BDNF/TrkB signaling regulates Purkinje cell spine number and morphology.
We will use the same in vitro system to test other signaling systems identified
in the genetic and genomic approaches above.
All of these approaches combine to give our
laboratory new and exciting ways to follow the signal transduction pathways
important for CNS neuronal survival, development, and synaptogenesis.
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