Abstract

The involvement of the N-methyl- d-aspartate (NMDA) subtype of glutamate receptors in the control of inspiratory termination was studied in paralyzed decerebrated cats. Cats were either vagotomized, or had intact vagus nerves and were ventilated with a ventilator driven by the discharge of the phrenic nerve. The systemic administration of NMDA antagonists acting non-competitively (MK-801, ketamine, phencyclidine) or competitively (2-amino-7-phosphonoheptanoic acid: AP7), produced an apneusis in vagotomized animals or in animals transiently deprived of vagal pulmonary feedback by the ‘no inflation test’. After NMDA receptor blockade, the inspiratory phase could be terminated by lung inflation or sensory stimulation. Thus pharmacologically distinct mechanisms control the termination of inspiration: vagal afferents which are NMDA-independent, and a central mechanism acting through the activation of NMDA receptors. The apneustic pattern induced by NMDA receptor blockade was characterized by a decrease of the amplitude of integrated phrenic nerve activity, the persistence of CO 2 sensitivity and an enhancement of apneusis by anaesthesia. After injection of NMDA antagonists there was a decrease of the duration of expiration which thereafter remained constant and dissociated from inspiratory duration. The possible mechanisms by which NMDA receptors may contribute to respiratory rhythmogenesis are discussed.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.