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Role of cAMP Cascade in Synaptic Stability and Plasticity: Ultrastructural and Physiological Analyses of Individual Synaptic Boutons in Drosophila Memory Mutants
Journal article   Open access   Peer reviewed

Role of cAMP Cascade in Synaptic Stability and Plasticity: Ultrastructural and Physiological Analyses of Individual Synaptic Boutons in Drosophila Memory Mutants

John J Renger, Atsushi Ueda, Harold L Atwood, C. K Govind and Chun-Fang Wu
The Journal of neuroscience, Vol.20(11), pp.3980-3992
06/01/2000
DOI: 10.1523/JNEUROSCI.20-11-03980.2000
PMCID: PMC6772635
PMID: 10818133
url
https://doi.org/10.1523/JNEUROSCI.20-11-03980.2000View
Published (Version of record) Open Access

Abstract

Mutations of the genes rutabaga (rut) and dunce (dnc) affect the synthesis and degradation of cAMP, respectively, and disrupt learning inDrosophila. Combined ultrastructural analysis and focal electrophysiological recording in the larval neuromuscular junction revealed a loss of stability and fine tuning of synaptic structure and function in both mutants. Increased ratios of docked/undocked vesicles and poorly defined synaptic specializations characterizeddnc synapses. In contrast, rut boutons possessed fewer, although larger, synapses with lower proportions of docked vesicles. At reduced Ca2+ levels, decreased quantal content coupled with an increase in failure rate was seen inrut boutons and reduced pair-pulse facilitation were found in both rut and dnc mutants. At physiological Ca2+ levels, strong enhancement, instead of depression, in evoked release was observed in somednc and rut boutons during 10 Hz tetanus. Furthermore, increased variability of synaptic transmission, including fluctuation and asynchronicity of evoked release, paralleled an increase in synapse size variation in both dnc andrut boutons, which might impose problems for effective signal processing in the nervous system. Pharmacological and genetic studies indicated broader ranges of physiological alteration bydnc and rut mutations than either the acute effects of cAMP analogs or the available mutations that affect cAMP-dependent protein kinase (PKA) activity. This is consistent with previous reports of more severe learning defects in dncand rut mutations than these PKA mutants and allows identification of the phenotypes involving long-term developmental regulation and those conferred by PKA.
 rut DCO ARTICLE dPKA-RI learning and memory neuromuscular junction Drosophila dnc vesicle docking synaptic ultrastructure variability and plasticity synaptic stability

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