Synaptic ultrastructure in nerve terminals of drosophila larvae overexpressing the learning gene dunce
We investigated synaptic ultrastructure of individual nerve ending varicosities at the Drosophila larval neuromuscular junction in transgenic larvae overexpressing the learning gene dunce (dnc) in the nervous system. It was previously shown that cAMP is reduced to one‐third normal in these larvae an...
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Veröffentlicht in: | Journal of neurobiology 2000-04, Vol.43 (1), p.89-97 |
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Sprache: | eng |
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Zusammenfassung: | We investigated synaptic ultrastructure of individual nerve ending varicosities at the Drosophila larval neuromuscular junction in transgenic larvae overexpressing the learning gene dunce (dnc) in the nervous system. It was previously shown that cAMP is reduced to one‐third normal in these larvae and that they have fewer nerve terminal varicosities and smaller junction potentials, although transmitter release from individual nerve ending varicosities is not significantly altered. We tested the hypothesis that synaptic ultrastructure is modified to compensate for possible reduced efficacy of synaptic transmission resulting from lower than normal cAMP. Synaptic size and number of presynaptic dense bodies (active zone structures) per synapse are modestly enhanced in transgenic larvae overexpressing the dnc gene product and in rutabaga (rut1 ) mutant larvae, which have reduced adenylyl cyclase activity and reduced neural cAMP. The incidence of complex synapses (possessing 2 or more presynaptic dense bodies) was not consistently different in experimental larvae compared to controls. The observations suggest that chronic reduction of cAMP levels in the nervous system of Drosophila larvae, although leading to a modest compensatory change in synaptic structure, does not markedly alter several synaptic ultrastructural parameters which are thought to influence the strength of transmitter release; thus, homeostatic mechanisms do not act to maintain normal‐sized junction potentials by altering synaptic structure. © 2000 John Wiley & Sons, Inc. J Neurobiol 43: 89–97, 2000 |
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ISSN: | 0022-3034 1097-4695 |
DOI: | 10.1002/(SICI)1097-4695(200004)43:1<89::AID-NEU8>3.0.CO;2-L |