The contribution of endogenous glutamatergic input in the ventral respiratory column to respiratory rhythm

Abstract Glutamate is the predominant excitatory neurotransmitter in the ventral respiratory column; however, the contribution of glutamatergic excitation in the individual subregions to respiratory rhythm generation has not been fully delineated. In an adult, in vivo, decerebrate rabbit model during conditions of mild hyperoxic hypercapnia we blocked glutamatergic excitation using the receptor antagonists 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX) and d(–)-2-amino-5-phosphonopentanoic acid (AP5). Disfacilitation of the preBotzinger Complex caused a decrease in inspiratory and expiratory duration as well as peak phrenic amplitude and ultimately apnea. Disfacilitation of the Botzinger Complex caused a decrease in inspiratory and expiratory duration; subsequent disfacilitation of the preBotzinger Complex resulted in complete loss of the respiratory pattern but maintained tonic inspiratory activity. We conclude that glutamatergic drive to the preBotzinger Complex is essential for respiratory rhythm generation. Glutamatergic drive to the Botzinger Complex significantly affects inspiratory and expiratory phase duration. Botzinger Complex neurons are responsible for maintaining the silent expiratory phase of the phrenic neurogram.