The role of central chemosensitivity in the control of ventilation in fishes was investigated directly by perfusing a mock extradural fluid (EDF) through the cranial space in the medullary region of conscious air-breathing fish, Amia calva. Perfusions with Sudan Black dye showed that the mock EDF communicated with the cerebrospinal fluid (CSF) and entered the cerebral ventricles. Altering the PO2, PCO2 and/or pH of the mock EDF had no effect on gill- or air-breathing rates, heart rate or blood pressure during exposure to normoxic water. Aquatic hypoxia, however, stimulated gill ventilation and elevated blood pressure, but did not affect heart rate; altering the gas tensions and/or pH of mock EDF still had no effect on recorded variables. Sodium cyanide (NaCN) added to the mock EDF caused struggling at concentrations above 500 μgml−1, but did not uniformly stimulate ventilation. These results suggest that central chemoreceptors, which mediate cardiovascular or ventilatory reflexes, are absent in Amia.

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