Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9743
Title: CCK-induced inhibition of presympathetic vasomotor neurons: dependence on subdiaphragmatic vagal afferents and central NMDA receptors in the rat.
Authors: Verberne, Anthony J M;Sartor, Daniela M
Affiliation: Clinical Pharmacology and Therapeutics Unit, Dept. of Medicine, Austin Health, Heidelberg, Victoria 3084, Australia. antonius@unimelb.edu.au
Issue Date: 20-May-2004
Citation: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 2004; 287(4): R809-16
Abstract: Systemic administration of cholecystokinin (CCK) inhibits a subpopulation of rostral ventrolateral medulla (RVLM) presympathetic vasomotor neurons. This study was designed to determine whether this effect involved subdiaphragmatic vagal afferents and/or central N-methyl-d-aspartic acid (NMDA) receptors. Recordings were made from CCK-sensitive RVLM presympathetic vasomotor neurons in halothane-anesthetized, paralyzed male Sprague-Dawley rats. The responses of the neurons to CCK (2 and 4 microg/kg iv), phenylephrine (PE; 5 microg/kg iv), and phenylbiguanide (PBG; 5 microg/kg iv) were tested before and after application of the local anesthetic lidocaine (2% wt/vol gel; 1 ml) to the subdiaphragmatic vagi at the level of the esophagus. In seven separate experiments, lidocaine markedly reduced the inhibitory effects of CCK on RVLM presympathetic neuronal discharge rate. In other experiments, the effect of systemic administration of dizocilpine (1 mg/kg iv), a noncompetitive antagonist at NMDA receptor ion channels, on the RVLM presympathetic neuronal responses to CCK, PBG, and PE was tested. In all cases (n = 6 neurons in 6 individual rats), dizocilpine inhibited the effects of CCK, PBG, and PE on RVLM presympathetic neuronal discharge. These results suggest that the effects of systemic CCK on the discharge of RVLM presympathetic neurons is mediated via an action on receptors located on subdiaphragmatic vagal afferents. Furthermore, the data suggest that CCK activates a central pathway involving NMDA receptors to produce inhibition of RVLM presympathetic neuronal discharge.
Internal ID Number: 15155283
URI: http://ahro.austin.org.au/austinjspui/handle/1/9743
DOI: 10.1152/ajpregu.00258.2004
URL: http://www.ncbi.nlm.nih.gov/pubmed/15155283
Type: Journal Article
Subjects: Adrenergic alpha-Agonists.pharmacology
Anesthetics, Local.pharmacology
Animals
Biguanides.pharmacology
Cholecystokinin.pharmacology
Depression, Chemical
Diaphragm.innervation.physiology
Dizocilpine Maleate.pharmacology
Excitatory Amino Acid Antagonists.pharmacology
Extracellular Space.drug effects.physiology
Male
Medulla Oblongata.cytology.drug effects.physiology
Motor Neurons.drug effects
Muscle, Smooth, Vascular.drug effects.innervation
Neurons, Afferent.physiology
Parasympathetic Nervous System.drug effects.physiology
Phenylephrine.pharmacology
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate.drug effects.physiology
Synaptic Transmission.drug effects
Vagus Nerve.physiology
Appears in Collections:Journal articles

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