Journal of Applied Physiology, Vol 50, Issue 2 239-244, Copyright © 1981 by American Physiological Society
Pharmacologic study of respiratory afterdischarge
D. E. Millhorn, F. L. Eldridge and T. G. Waldrop
Respiratory afterdischarge, an increased but slowly declining respiratory
output lasting some minutes after cessation of a stimulus, is generated by
a bulbopontine mechanism whose precise anatomic locus and
neurophysiological mechanism are unknown. To determine if the mechanism
responsible for the afterdischarge was due to one of the major long-acting
central neurotransmitters, we studied a control group of animals and groups
of animals that were pretreated with the antiserotonin agents,
methysergide, parachlorophenylalanine, and 5,7-dihydroxytryptamine, the
dopamine-norepinephrine antagonists alpha-methytyrosine and haloperidol,
and the endorphin antagonist, naloxone. Anesthetized, paralyzed,
vagotomized, and glomectomized cats were used. We measured phrenic activity
before, during, and after carotid sinus nerve and calf muscle stimulation.
None of the antagonists had an effect on the response to stimulation, on
the magnitude of the afterdischarge, or on its time course during recovery.
We conclude that these central neurotransmitters do not participate in the
genesis of the respiratory afterdischarge.
