Potassium current in Drosophila neurons is increased by either dunce mutation or cyclic AMP

In the Drosophila mutant dunce, short‐term memory is deficient and intracellular cyclic adenosine monophosphate (cAMP) concentration is elevated. We examined the effect of increased cAMP concentration on the potassium current. The conventional whole‐cell technique was applied to cultured “giant” Dro...

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Bibliographic Details
Published in:Journal of neuroscience research 1998-06, Vol.52 (5), p.521-529
Main Authors: Alshuaib, Waleed B., Mathew, Mini V.
Format: Article
Language:English
Subjects:
Animals
Bucladesine - pharmacology
Cyclic AMP - physiology
Drosophila melanogaster
Drosophila melanogaster - embryology
Drosophila melanogaster - genetics
Drosophila melanogaster - physiology
Electric Conductivity
learning mutants
Memory, Short-Term - physiology
modulation
Mutation - physiology
Neurons - drug effects
Neurons - physiology
patch-clamp
Patch-Clamp Techniques
Potassium - physiology
Theophylline - pharmacology
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Summary:In the Drosophila mutant dunce, short‐term memory is deficient and intracellular cyclic adenosine monophosphate (cAMP) concentration is elevated. We examined the effect of increased cAMP concentration on the potassium current. The conventional whole‐cell technique was applied to cultured “giant” Drosophilaneurons derived from cell‐division arrested embryonic neuroblasts. Potassium membrane currents were measured from: 1) control wild‐type neurons, 2) wild‐type neurons with dibutyryl cAMP and theophylline in the culture media for 2 days (db‐cAMP‐treated), and 3) dunceneurons. Delayed‐rectifier potassium current was greater in both dunceneurons and db‐cAMP‐treated wild‐type neurons than in control wild‐type neurons. This result indicates that the neuronal potassium current is increased by the long‐term increase of cAMP. Conceivably, altered neuronal excitability in the dunce mutant could disrupt the processing of neural signals necessary for learning and memory. J. Neurosci. Res. 52:521–529, 1998. © 1998 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/(SICI)1097-4547(19980601)52:5<521::AID-JNR4>3.0.CO;2-E