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Breathing is highly sensitive to the PCO 2  of arterial blood. Although CO 2  is detected via the proxy of pH, CO 2  acting directly via Cx26 may also contribute to the regulation of breathing. Here we exploit our knowledge of the structural motif of CO 2 -binding to Cx26 to devise a dominant negative subunit (Cx26 DN ) that removes the CO 2 -sensitivity from endogenously expressed wild type Cx26. Expression of Cx26 DN  in glial cells of a circumscribed region of the mouse medulla - the caudal parapyramidal area – reduced the adaptive change in tidal volume and minute ventilation by approximately 30% at 6% inspired CO 2 . As central chemosensors mediate about 70% of the total response to hypercapnia, CO 2 -sensing via Cx26 in the caudal parapyramidal area contributed about 45% of the centrally-mediated ventilatory response to CO 2 . Our data unequivocally link the direct sensing of CO 2  to the chemosensory control of breathing and demonstrates that CO 2 -binding to Cx26 is a key transduction step in this fundamental process.

Connexin26 mediates CO2-dependent regulation of breathing via glial cells of the medulla oblongata