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ARTICLE |
Cellular/Molecular
Exploring Neurodegeneration with Drosophila Mutants
blue cheese Mutations Define a Novel,
Conserved Gene Involved in Progressive Neural Degeneration
Kim D. Finley, Philip T. Edeen, Robert C. Cumming,
Michelle D. Mardahl-Dumesnill, Barbara J. Taylor, Maria H. Rodriguez,
Calvin E. Hwang, Michael Benedetti, and Michael
McKeown (see pages 1254-1264)
Neural Dysfunction and Neurodegeneration in
Drosophila Na+/K+ ATPase
Alpha Subunit Mutants
Michael J. Palladino, Jill E. Bower, Robert Kreber, and Barry
Ganetzky (see pages 1276-1286)
Model organisms such as Drosophila are receiving
increased attention for studies of human neurodegenerative disease.
Although the merit of such systems for genetic studies is apparent, the relevance of a neurodegenerative phenotype in flies, whose lifespan is
measured in weeks, to the long duration of human neurodegenerative diseases would seem less clear. However, two articles in this issue of
the Journal provide additional evidence for the
potential value of such studies. Finley et al. describe a novel
loss-of-function mutant, blue cheese, that has a reduced
life span, protein aggregates in the neuropil of "aged" animals,
and neuronal apoptosis. The blue cheese protein, whose function is
unknown, is expressed in the cytoplasm of CNS neurons and has a human
homolog. In contrast, Palladino et al. report a neurodegenerative
phenotype in Drosophila with mutations in a known
protein, the
subunit of the Na/K ATPase. The sodium pump is
fundamental to the maintenance of ion gradients in normal
neurons. These mutants, identified in a screen for
temperature-sensitive paralytic mutants, showed age-dependent,
spongioform neurodegeneration but did not show protein aggregates. The
mutations caused a reduced life span but could also cause
hyperexcitability and seizures.
Development/Plasticity/Repair
Micromodular Organization in Cerebral Cortex
Honeycomb-Like Mosaic at the Border of Layers 1 and 2 in the
Cerebral Cortex
Noritaka Ichinohe, Fumino Fujiyama, Takeshi Kaneko, and Kathleen
S. Rockland (see pages 1372-1382)
It is unusual these days for research studies to report
new neuroanatomical features in brain. However, Ichinohe et al. used parvalbumin staining to reveal small (<100 µm) honeycomb-like structures, restricted to the border of layers 1 and 2 of rat visual
cortex. The honeycombs were composed of intermingled dendritic bundles
of GABAergic interneurons and pyramidal cells, zinc-rich corticocortical (CC) afferents, and thalamocortical (TC) nerve terminals. The honeycomb walls stained with parvalbumin as well as NMDA
receptor 1 and glutamate receptor 1 receptor subunits. The
laminar-specific substructures were also present in cat and monkey
cortex and exhibited a high degree of regularity. The honeycomb organization appears to segregate CC and TC inputs into distinct dendritic compartments. Although the function of honeycomb organization remains unknown, the authors suggest that CC and TC represent two
parallel systems in layer 2 that target different populations of
pyramidal cell dendrites.

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Labeling for microtubule-associated protein 2 (MAP2)
(green) shows apical dendrites of pyramidal cells that
end near the border of layers 1 and 2. The dendrites are surrounded by
the parvalbumin-immunoreactive fibers (red) in the walls
of each honeycomb.
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