Neuroblast ablation in Drosophila P[GAL4] lines reveals origins of olfactory 
interneurons

Stocker, RF; Heimbeck, G; Gendre, N; de Belle, JS

doi:10.1002/(SICI)1097-4695(199705)32:5<443::AID-NEU1>3.0.CO;2-5

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Neuroblast ablation in Drosophila P[GAL4] lines reveals origins of olfactory interneurons

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de Belle, JS
Former Department Neurophysiology of Insect Behavior, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

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https://onlinelibrary.wiley.com/doi/epdf/10.1002/%28SICI%291097-4695%28199705%2932%3A5%3C443%3A%3AAID-NEU1%3E3.0.CO%3B2-5
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Citation

Stocker, R., Heimbeck, G., Gendre, N., & de Belle, J. (1997). Neuroblast ablation in Drosophila P[GAL4] lines reveals origins of olfactory interneurons. Journal of Neurobiology, 32(5), 443-456. doi:10.1002/(SICI)1097-4695(199705)32:5<443:AID-NEU1>3.0.CO;2-5.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0013-EA9E-4

Abstract

Hydroxyurea (HU) treatment of early first instar larvae in Drosophila was previously shown to ablate a single dividing lateral neuroblast (LNb)
in the brain. Early larval HU application to p[GAL4] strains that label specific neuron types enabled us to identify the origins of the two major classes of
interneurons in the olfactory system. HU treatment resulted in the loss of antennal lobe local interneurons and of a subset of relay interneurons (RI),
elements usually projecting to the calyx and the lateral protocerebrum (LPR). Other RI were resistant to HU and still projected to the ERR. However, they
formed no collaterals in the calyx region (which was also ablated), suggesting that their survival does not depend on targets in the calyx. Hence, the
ablated interneurons were derived from the LNb, whereas the HU-resistant elements originated from neuroblasts which begin to divide later in larval life.
Developmental GAL4 expression patterns suggested that differentiated RI are present at the larval state already and may be retained through
metamorphosis. (C) 1997 John Wiley Sons, Inc.