Interactions Between Carbon Dioxide and Oxygen Sensing in the Control of Locust Ventilatory Pattern Generation


Meeting Abstract

P2-71  Saturday, Jan. 5 15:30 – 17:30  Interactions Between Carbon Dioxide and Oxygen Sensing in the Control of Locust Ventilatory Pattern Generation AYALI, A*; TALAL, S; GEFEN, E; Tel Aviv University; Tel Aviv University; University of Haifa-Oranim ayali@post.tau.ac.il https://www.tau.ac.il/~ayali/

Insects exchange respiratory gases through an extensive network of tracheae that open to the surface of the body via segmental spiracles. In actively ventilating insects, such as the locust, respiration involves the well-coordinated activity of spiracular muscles and ventilatory muscles, responsible for abdominal pumping movements. Our previously reported data indicated a strong coupling between the spiracular and the ventilation pattern generating circuits (CPG), and provided insights into their modulation by concentrations of respiratory gases. Here, we directly tested the interactions between CO2 and O2 sensing in the control of the locust ventilatory motor patterns through in-vitro isolation of the thoracic ganglia, where ventilatory CPG are located, and their associated main tracheae. We perfused the main tracheae with various gases mixtures while recording the rhythmic activity from the motor nerves controlling spiracle and ventilatory muscles. Initially, using aerated saline we recorded no change in the fictive ventilatory activity to increasing tracheal CO2 levels (at 6% O2) within the physiologically relevant range. In contrast, when the saline was bubbled with 6% O2 in N2 (or in anoxic saline), a significant increase was recorded at 3.5% CO2, indicating a role for hemolymph gas concentration. Reducing tracheal O2 levels (in 0% CO2 ) resulted in significantly increased ventilatory activity only at 2% O2. However, the response to 3.5% CO2 was significantly higher at tracheal levels of 3% O2, and lower at 9% O2, compared with 6% O2. Furthermore, efferent ventilatory output increased 3-fold at 2% O2 and 2% CO2, whereas 2% O2 alone caused a 20% increase only and 2% CO2 alone did not elicit any response. Together, these findings indicate central sensing of both respiratory gases, and interaction in their effects on respiratory output from the CNS.

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