Faculty Collaboration Database

NMDA receptor-mediated transmission of carotid body chemoreceptor input to expiratory bulbospinal neurones in dogs. J Physiol 1995 Sep 15;487 ( Pt 3)(Pt 3):639-51

Date

09/15/1995

Pubmed ID

8544127

Pubmed Central ID

PMC1156651

DOI

10.1113/jphysiol.1995.sp020906

Scopus ID

2-s2.0-0029116655 (requires institutional sign-in at Scopus site)   42 Citations

Abstract

1. This study tested the hypothesis that excitatory amino acid receptors mediate the excitatory response of expiratory bulbospinal neurones to carotid body chemoreceptor inputs. 2. Studies were carried out in thiopental sodium anaesthetized, paralysed, ventilated, vagotomized dogs. 3. Brisk, short-duration chemoreceptor activation was produced by bilateral bolus injections of CO2-saturated saline (PCO2 > 700 mmHg) into the autoperfused carotid arteries. A pressurized-reservoir-solenoid valve system was used to deliver the CO2 bolus injections just prior to the onset of the neural expiratory phase, as determined from the phrenic neurogram, about once per minute. 4. Multibarrelled micropipettes were used to record neuronal unit activity and deliver neurotransmitter agents. Net responses of expiratory bulbospinal neurones to peripheral chemoreceptor activation were determined by subtracting the mean discharge frequencies (Fn) during three control expiratory cycles from the Fn during administration of a CO2 test bolus. The role of excitatory amino acid receptors in mediating this response was determined by comparing the baseline and bolus expiratory neuronal Fn before, during and after the pressure microejection of the NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP5) or the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulphamoyl- benzo(f)quinoxaline (NBQX). Ejection rates of AP5 and NBQX were measured by monitoring the movement of the pipette meniscus. 5. AP5 reduced Fn during both the control and bolus cycles, as well as reducing the change in Fn between control and bolus cycles. NBQX had no effect on either baseline or bolus responses. 6. AP5 did not prevent excitation of expiratory bulbospinal neurones by AMPA. Coadministration of AMPA with AP5 prevented the AP5-mediated decrease in Fn but not the dose-dependent reduction in the CO2 bolus response. 7. Taken together, these data strongly suggest that the carotid chemoreceptor-mediated excitation of expiratory bulbospinal neurones is dependent on NMDA but not non-NMDA glutamate receptors.

Author List

Dogas Z, Stuth EA, Hopp FA, McCrimmon DR, Zuperku EJ

Authors

Eckehard A. Stuth MD Professor in the Anesthesiology department at Medical College of Wisconsin
Edward J. Zuperku PhD Professor in the Anesthesiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

2-Amino-5-phosphonovalerate
Animals
Carbon Dioxide
Carotid Body
Dogs
Excitatory Amino Acid Agonists
Excitatory Amino Acid Antagonists
Female
Male
Medulla Oblongata
Microinjections
Neurons
Quinoxalines
Receptors, N-Methyl-D-Aspartate
Respiratory Mechanics
Spinal Cord
Stimulation, Chemical
Synaptic Transmission
Vagotomy
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid