Synaptic ultrastructure in nerve terminals of Drosophila larvae overexpressing the learning gene dunce

Citation
Aj. Shayan et Hl. Atwood, Synaptic ultrastructure in nerve terminals of Drosophila larvae overexpressing the learning gene dunce, J NEUROBIOL, 43(1), 2000, pp. 89-97
Citations number
36
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROBIOLOGY
ISSN journal
00223034 → ACNP
Volume
43
Issue
1
Year of publication
2000
Pages
89 - 97
Database
ISI
SICI code
0022-3034(200004)43:1<89:SUINTO>2.0.ZU;2-5
Abstract
We investigated synaptic ultrastructure of individual nerve ending varicosi ties at the Drosophila larval neuromuscular junction in transgenic larvae o verexpressing the learning gene dunce (dnc) in the nervous system. It was p reviously shown that cAMP is reduced to one-third normal in these larvae an d that they have fewer nerve terminal varicosities and smaller junction pot entials, although transmitter release from individual nerve ending varicosi ties is not significantly altered. We tested the hypothesis that synaptic u ltrastructure is modified to compensate for possible reduced efficacy of sy naptic transmission resulting from lower than normal cAMP. Synaptic size an d number of presynaptic dense bodies (active zone structures) per synapse a re modestly enhanced in transgenic larvae overexpressing the dnc gene produ ct and in rutabaga (rut(1)) mutant larvae, which have reduced adenylyl cycl ase activity and reduced neural cAMP. The incidence of complex synapses (po ssessing 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 larva e, although leading to a modest compensatory change in synaptic structure, does not markedly alter several synaptic ultrastructural parameters which a re thought to influence the strength of transmitter release; thus, homeosta tic mechanisms do not act to maintain normal-sized junction potentials by a ltering synaptic structure. (C) 2000 John Wiley & Sons, Inc. J Neurobiol 43 : 89-97, 2000.