The central chemoreceptor drive to ventilation was assessed in unanesthetized toads, Bufo paracnemis, exposed to three different temperatures: 15, 25 and 35 degrees C. The acid-base status of the fourth ventricle was manipulated by mock CSF perfusion. In additional experiments, arterial pH was varied by inspiration of hypercapnic gas mixtures. Ventilation was measured directly by pneumotachography and arterial blood samples were analyzed using electrodes for pH and PO2. Regardless of temperature, the ventilatory control of acid-base status was predominantly central. Moreover, an increase in temperature was accompanied by a proportional increase in the ventilatory response to chemoreceptor stimulation by either lowered mock CSF pH or hypercapnia. The alphastat hypothesis could not adequately account for the temperature effects on the ventilatory responses to hypercapnia or on air convection requirements in the toad.