6533b81ffe1ef96bd1279065

RESEARCH PRODUCT

Evidence for a respiration-modulated cholinergic action on the activity of medullary respiration-related neurons in the rabbit. An iontophoretic study.

M. BaumannKurt SchmidG. Böhmer

subject

medicine.medical_specialtyPhysiologyClinical BiochemistryRespiratory SystemAction PotentialsBethanecholHexamethonium CompoundsInhibitory postsynaptic potentialHexamethoniumchemistry.chemical_compoundBethanechol CompoundsPhysiology (medical)Internal medicineMuscarinic acetylcholine receptormedicineAnimalsNeurotransmitterNeuronsRespirationBethanecholIontophoresisReceptors MuscarinicAcetylcholineElectrophysiologyNicotinic agonistmedicine.anatomical_structureEndocrinologychemistryCholinergicNeuronRabbitsDimethylphenylpiperazinium IodideAcetylcholinemedicine.drug

description

Effects of the iontophoretically administered cholinergic agonists acetylcholine, bethanechol and DMPP on the activity of medullary respiration-related neurons were examined in urethane-anaesthetized rabbits. Inhibitory effects prevailed over excitatory effects. Analysis of cholinergic effects by cycle-triggered averaging revealed three major types of neuronal responses: (i) constant alterations of spike-density throughout the whole period of activity ("constant effects"), (ii) effects increasing during the progression of the burst of discharge or effects restricted to a particular fraction of the burst ("phasic effects") and (iii) effects which were characterized by an excitation during one respiratory phase and an inhibition during the other phase ("bi-phasic effects"). The latter type of effects was observed in phase-spanning respiration-related neurons. Phasic effects were mainly observed in inspiration-related neurons which were predominantly inhibited by stimulation of muscarinic receptors. Inspiratory R beta-neurons in no case were phasically affected by cholinergic agents. The mean muscarinic inhibition of inspiration-related neurons increased with the progression of inspiration. The mean nicotinic inhibition of expiration-related neurons decreased with the progression of expiration. Results suggest that the efficacy of (i) a central inspiration terminating mechanism and (ii) the onset of discharge of expiratory neurons is modulated by acetylcholine.

10.1007/bf00373143https://pubmed.ncbi.nlm.nih.gov/2576119