SEROTONIN 1A-RECEPTOR ACTIVATION SUPPRESSES RESPIRATORY APNEUSIS IN THE CAT

Malfunction of inhibitory synaptic processes in the brainstem result i n abnormal prolonged inspiration (apneusis). Since we previously found that the serotonin (5-hydroxytryptamine; 5-HT) 5-HT1A receptor agonis t 8-hydroxy-dipropylaminotetralin (8-OH-DPAT) shortens inspiratory dis charges, we tested its ability to suppress apneusis. We recorded phren ic nerve activity and the membrane potential of medullary expiratory ( E-2) and postinspiratory (PI) neurons in 14 anaesthetized, paralyzed, artifically ventilated cats. Systemic hypoxia or i.v. injection of pen tobarbital sodium or the N-methyl-D-aspartate (NMDA) receptor blocker ketamine induced apneustic phrenic nerve discharges, delayed depolariz ation to threshold of E-2 neurons and prolonged hyperpolarization in P I neurons. 8-OH-DPAT (10-40 mu g/kg i.v.) produced partial to complete restoration of normal phrenic nerve discharges and membrane potential .