Effect of reduced impulse activity on the development of identified motor terminals in Drosophila larvae.
In Drosophila larvae, motoneurons show distinctive differences in the size of their synaptic boutons; that is, axon 1 has type Ib ("big" boutons) terminals and axon 2 has type Is ("small" boutons) terminals on muscle fibers 6 and 7. To determine whether axon 1 develops large boutons due to its high impulse activity, we reduced impulse activity and examined the motor terminals formed by axon 1. The number of functional Na(+) channels was reduced either with the nap(ts) mutation or by adding tetrodotoxin (TTX) to the media (0.1 microg/g). In both cases, the rate of locomotion was decreased by approximately 40%, presumably reflecting a decrease in impulse activity. Locomotor activity was restored to above wild-type (Canton-S) levels when nap(ts) was combined with a duplication of para, the Na(+)-channel gene. Lucifer yellow was injected into the axon 1 motor terminals, and we measured motor terminal area, length, the number of branches, and the number and width of synaptic boutons. Although all parameters were smaller in nap(ts) and TTX-treated larvae compared to wild-type, most of these differences were not significant when the differences in muscle fiber size were factored out. Only bouton width was significantly smaller in both different nap(ts) and TTX-treated larvae: boutons were about 20% smaller in nap(ts) and TTX-treated larvae, and 20% larger in nap(ts); Dp para(+) compared to wild-type. In addition, terminal area was significantly smaller in nap(ts) compared to wild-type. Bouton size at Ib terminals with reduced impulse activity was similar to that normally seen at Is terminals. Thus, differences in impulse activity play a major role in the differentiation of bouton size at Drosophila motor terminals.
Lnenicka
Gregory A
GA
Department of Biological Sciences, University at Albany, SUNY, Albany, New York 12222, USA. gregL@albany.edu
Spencer
Gregory M
GM
Keshishian
Haig
H
D000818:Animals; D030801:Animals, Genetically Modified; D001369:Axons / Q000145:classification / Q000502:physiology / Q000648:ultrastructure; D004331:Drosophila melanogaster / Q000502:physiology*; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials; D006735:Horseradish Peroxidase; D007546:Isoquinolines; D007814:Larva / Q000254:growth & development / Q000502:physiology*; D009043:Motor Activity / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D009046:Motor Neurons / Q000145:classification / Q000502:physiology*; D015999:Multivariate Analysis; D009132:Muscles / Q000294:innervation*; D009154:Mutation; D009411:Nerve Endings / Q000187:drug effects / Q000502:physiology; D009469:Neuromuscular Junction / Q000166:cytology / Q000502:physiology*; D009473:Neuronal Plasticity; D017729:Presynaptic Terminals / Q000187:drug effects / Q000648:ultrastructure; D013779:Tetrodotoxin / Q000494:pharmacology
D007546:Isoquinolines; D013779:Tetrodotoxin; C017475:lucifer yellow; D006735:Horseradish Peroxidase