Although respiratory motor output is controlled in the brainstem, ventilation and its responses to hypoxia are also dependent on the higher brain status. In the present study, we aimed to explore the relationship between the higher brain function and ventilatory responses to mild and severe hypoxia. We simultaneously analyzed the higher brain status and ventilatory parameters in unanesthetized adult mice by EEG and whole body plethysmography, respectively. Screw electrodes for EEG recording were secured in the skull, which targeted at 2.5 mm anterior and 2.5 mm posterior to the bregma. Two-channel EEG signals from the anterior and posterior electrodes were recorded at 400 Hz sampling, and bandpass filtered at 0.1-100 Hz. Digital power spectrogram was generated by a fast Fourier transform from the filtered EEG waveform, and its respiration-triggered averaging was performed. In whole body plethysmography, respiratory flow was measured at 400 Hz sampling and bandpass filtered at 0.1-20 Hz. We then calculated tidal volume, respiratory rate and minute ventilation. For the analysis of ventilatory responses to hypoxia, mice breathed first room air, then mild (12% O₂ in N₂) or severe (6% O₂ in N₂) hypoxic gas, and again room air. In the room air condition, EEG signals recorded from the anterior electrodes were respiration-synchronized, but those from the posterior electrodes were not. Mild hypoxia persistently increased ventilation. Severe hypoxia initially increased ventilation, but then induced suppression of ventilation together with inhibition of EEG signals. It could be explained by a reduction of central command from the higher brain to the brainstem respiratory center. This mechanism may underlie the pathophysiology of respiratory arrest in cases loaded with severe acute hypoxia.