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Pharmacological analysis of heartbeat in Drosophila
1Department of Biochemical Pharmacology, State University of New York at Buffalo 14260, USA.
Insights
Drosophila heartbeats are myogenic and influenced by calcium and potassium channels, not sodium channels. This study introduces a simple preparation for studying cardiac excitability and identifying related mutations in fruit flies.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Genetics
Background:
- Understanding cardiac excitability mechanisms is crucial.
- Drosophila melanogaster offers a valuable genetic model for studying ion channels and receptors.
- Previous limitations included a lack of suitable heart preparations and knowledge of ionic currents in Drosophila.
Purpose of the Study:
- To develop a simple preparation for measuring Drosophila heartbeat.
- To investigate if Drosophila heartbeat is myogenic.
- To identify ion channels influencing Drosophila heart rate.
Main Methods:
- Developed a novel, simple preparation for Drosophila heart monitoring.
- Administered tetrodotoxin to assess sodium channel involvement.
- Applied L-type calcium channel blockers (PN200-110, verapamil, diltiazem) and potassium channel blockers (tetraethylammonium, quinidine).
Main Results:
- Tetrodotoxin did not affect heart rate, suggesting a myogenic origin and no significant role for Na+ channels.
- Heart rate was modulated by L-type calcium channel blockers, indicating their involvement.
- Potassium channel blockers affected heart rate, suggesting a role for K+ currents.
Conclusions:
- Drosophila heartbeat is likely myogenic and influenced by L-type calcium and potassium channels.
- The developed preparation is effective for studying cardiac excitability and identifying relevant mutations in Drosophila.
- Findings suggest conserved roles of certain ion channels in cardiac function across species.
Abstract:
Analysis of the mechanisms underlying cardiac excitability can be facilitated greatly by mutations that disrupt ion channels and receptors involved in this excitability. With an extensive repertoire of such mutations, Drosophila provides the best available genetic model for these studies. However, the use of Drosophila for this purpose has been severely handicapped by lack of a suitable preparation of heart and a complete lack of knowledge about the ionic currents that underlie its excitability. We describe a simple preparation to measure heartbeat in Drosophila. This preparation was used to ask if heartbeat in Drosophila is myogenic in origin, and to determine the types of ion channels involved in influencing the heart rate. Tetrodotoxin, even at a high concentration of 40 microM, did not affect heart rate, indicating that heartbeat may be myogenic in origin and that it may not be determined by Na+ channels. Heart rate was affected by PN200-110, verapamil, and diltiazem, which block vertebrate L-type Ca2+ channels. Thus, L-type channels, which contribute to the prolonged plateau of action potentials in vertebrate heart, may play a role in Drosophila cardiac excitability. It also suggests that Drosophila heart is subject to a similar intervention by organic Ca2+ channel blockers as the vertebrate heart. A role for K+ currents in the function of Drosophila heart was suggested by an effect of tetraethylammonium, which blocks all the four identified K+ currents in the larval body wall muscles, and quinidine, which blocks the delayed rectifier K+ current in these muscles. The preparation described here also provides an extremely simple method for identifying mutations that affect heart rate. Such mutations and pharmacological agents will be very useful for analyzing molecular components of cardiac excitability in Drosophila.