Serotonin 1A-receptor activation suppresses respiratory apneusis in the cat.

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