Z. Dogas et al., NMDA RECEPTOR-MEDIATED TRANSMISSION OF CAROTID-BODY CHEMORECEPTOR INPUT TO EXPIRATORY BULBOSPINAL NEURONS IN DOGS, Journal of physiology, 487(3), 1995, pp. 639-651
1. This study tested the hypothesis that excitatory amino acid recepto
rs mediate the excitatory response of expiratory bulbospinal neurones
to carotid body chemoreceptor inputs. 2. Studies mere carried out in t
hiopental sodium anaesthetized, paralysed, ventilated, vagotomized dog
s. 3. Brisk, short-duration chemoreceptor activation nas produced by b
ilateral bolus injections of CO2-saturated saline (P-Co2 > 700 mmHg) i
nto the autoperfused carotid arteries. A pressurized-reservoir-solenoi
d valve system was used to deliver the CO2 bolus injections just prior
to tile onset of the neural expiratory phase, as determined from the
phrenic neurogram, about once per minute. 4. Multibarrelled micropipet
tes mere used to record neuronal unit activity and deliver neurotransm
itter agents. Net responses of expiratory bulbospinal neurones to peri
pheral chemoreceptor activation were determined by subtracting the mea
n discharge frequencies (F-n) during three control expiratory cycles f
rom the F-n during administration of a CO2 test bolus. The role of exc
itatory amino acid receptors in mediating this response was determined
by comparing the baseline and bolus expiratory neuronal F-n before, d
uring and after the pressure microejection of the NMDA receptor antago
nist 2-amino-5-phosphonovalerate (AP5) or the non-NMDA receptor antago
nist dihydroxy-6-nitro-7-sulphamoyl-benzo(f)quinoxaline (NBQX). Ejecti
on rates of AP5 and NBQX were measured by monitoring the movement of t
he pipette meniscus. 5. AP5 reduced F-n during both the control and bo
lus cycles, as well as reducing the change in F-n between control and
bolus cycles. NBQX had no effect on either baseline or bolus responses
. 6. AP5 did not prevent excitation of expiratory bullospinal neurones
by AMPA. Coadministration of AMPA with AP5 prevented the AP5-mediated
decrease in F-n but not the dose-dependent reduction in the CO2 bolus
response. 7. Taken together, these data strongly suggest that the car
otid chemoreceptor-mediated excitation of expiratory bulbospinal neuro
nes is dependent on NMDA but not non-NMDA glutamate receptors.