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Temperate Drosophila preserve cardiac function at low temperature.

Jonas Lembcke Andersen1, Heath Andrew MacMillan1, Johannes Overgaard1

  • 1Zoophysiology, Department of Bioscience, Aarhus University, DK-8000 Aarhus, Denmark.

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Insect heart function is crucial for surviving cold temperatures. This study reveals that temperate Drosophila species maintain cardiac performance at lower temperatures than tropical ones, highlighting the importance of nervous system input for cold tolerance.

Keywords:
Central nervous systemChill toleranceDecapitated fliesDrosophila heart rateMuscle function

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Area of Science:

  • Zoology
  • Insect Physiology
  • Environmental Biology

Background:

  • Insects enter chill coma at low temperatures, linked to neuromuscular failure.
  • Insect heart rate (HR) is regulated by intrinsic pacemakers and extrinsic nervous/humoral input.

Purpose of the Study:

  • Investigate the relationship between cardiac performance and cold tolerance (CTmin) in five Drosophila species.
  • Differentiate the effects of cold on intrinsic vs. extrinsic HR regulation.

Main Methods:

  • Measured HR-temperature relationships in five Drosophila species.
  • Assessed cardiac performance via Arrhenius break point (ABP) and HR cessation temperature.
  • Examined HR in decapitated flies and amputated abdomens of Drosophila montana to isolate extrinsic input.

Main Results:

  • Found strong correlations between HR-ABP, HR cessation temperature, and whole-animal CTmin across species.
  • Temperate Drosophila species exhibited superior cardiac function at lower temperatures compared to tropical species.
  • Isolated hearts (reduced extrinsic input) showed higher thermal sensitivity and lower ABP, indicating neuronal input is vital for low-temperature HR stimulation.

Conclusions:

  • Cardiac performance is a key determinant of insect cold tolerance.
  • Central nervous system input plays a critical role in maintaining insect heart rate at low temperatures.
  • Drosophila species adapted to temperate climates possess enhanced cardiac mechanisms for cold survival.