1. Interneurones located in the circumoesophageal commissures were found to control the activity of the cardioinhibitor and cardioaccelerator regularity neurones. 2. These interneurones (cardiac command fibres) fell into three classes: (1) strong inhibitors, which caused cardiac arrest, (2) weak inhibitors, which caused bradycardia, and (3) accelerators, which caused tachycardia. 3. When the positions of interneurones were plotted collectively, they formed distinct clusters, suggesting that each cluster was represented by one command unit in an individual preparation. Twenty strong inhibitor units and 16 accelerator units were found. Weak inhibitors did not form clusters. 4. Stimulus threshold characteristics were as low as 3.0 V and 3 Hz for the strong inhibitor units (mean range 4.7-7.1 V and 14–30 Hz). Higher values were found for weak inhibitors and accelerators. 5. The strong inhibitor command drives always showed a positive bias toward the contralateral cardioinhibitor neurone, relative to the ipsilateral cardioinhibitor. 6. Plots of command neurone stimulating frequency versus evoked cardio-inhibitor activity displayed steep positive slopes for strong inhibitor command units and shallow positive slopes for weak inhibitor units. 7. Reciprocity between the cardioinhibitor and cardioaccelerator neurones occurred during both inhibitory and acceleratory command drives. This is not likely to be a property inherent in the command units themselves because reciprocity was earlier observed during chemical and tactile reflex inhibition of the heart. (Field & Larimer, 1974a).

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