1. Our purpose was to define whether a region of medulla could be identified that is critical for the expression of gasping. 2. Decerebrate, vagotomized, paralysed and ventilated adult rats were used. The pattern of phrenic activity was reversibly altered from eupnoea to gasping by exposure to hypoxia or anoxia. 3. Gasping was irreversibly eliminated following unilateral electrolytic lesions of the lateral tegmental field of the medulla. The eupnoeic rhythm continued after these lesions. 4. Injections of kainic acid into the lateral tegmental field also eliminated gasping. Phrenic activity in eupnoea was not altered. 5. Lesions outside the lateral tegmental field caused marked changes in the eupnoeic rhythm, including expiratory apnoea. Upon exposure to hypoxia or anoxia, gasping was still induced. 6. This region for the neurogenesis of gasping in rats is identical to the region that serves a comparable function in cats. Moreover, it overlaps with the ‘pre‐Bötzinger’ complex which has been described for the in vitro brainstem preparation of the neonatal rat. Our results raise doubts that this complex plays a role in the neurogenesis of eupnoea.

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