A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Griffith, L.C., Verselis, L.M., Aitken, K.M., Kyriacou, C.P., Danho, W., Greenspan, R.J. (1993). Inhibition of calcium/calmodulin-dependent protein kinase in Drosophila disrupts behavioral plasticity.  Neuron 10(3): 501--509. (Export to RIS)
FlyBase ID FBrf0059167
Publication Type Research paper
PubMed ID 8384859
PubMed Abstract One of the major mediators of calcium action in neurons is the multifunctional calcium/calmodulin-dependent protein kinase (CaM kinase), an enzyme with the capability of directly regulating its own activity by autophosphorylation. To assess the involvement of CaM kinase in experience-dependent behavior in an intact animal, we have designed a specific peptide inhibitor of CaM kinase and made transgenic Drosophila that express it under control of an inducible promoter. These flies fail to learn normally in two behavioral plasticity paradigms: acoustic priming, a nonassociative measure of sensitization, and courtship conditioning, a measure of associative learning. The magnitude of the learning defect in the associative paradigm appears to be proportional to the level of expression of the peptide gene in the two transgenic lines and can be increased by heat shock induction of gene expression. These results suggest that CaM kinase activity is required for plastic behaviors in an intact animal.
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Secondary IDs FBrf0073233
Language of Publication English
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Publication Type Journal
Abbreviation Neuron
Title Neuron
Publication Year 1988-
ISBN/ISSN 0896-6273
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