TY - JOUR
T1 - Relative magnitude of tonic and phasic synaptic excitation of medullary inspiratory neurons in dogs
AU - Krolo, M.
AU - Stuth, E. A.
AU - Tonkovic-Capin, M.
AU - Hopp, F. A.
AU - McCrimmon, D. R.
AU - Zuperku, E. J.
PY - 2000
Y1 - 2000
N2 - The relative contribution of phasic and tonic excitatory synaptic drives to the augmenting discharge patterns of inspiratory (I) neurons within the ventral respiratory group (VRG) was studied in anesthetized, ventilated, paralyzed, and vagotomized dogs. Multibarrel micropipettes were used to record simultaneously single-unit neuronal activity and pressure micro-ejected antagonists of GABAergic, glycinergic, N-methyl-D-aspartate (NMDA) and non-NMDA glutamatergic, and cholinergic receptors. The discharge patterns were quantified via cycle-trigger histograms. The findings suggest that two-thirds of the excitatory drive to caudal VRG I neurons is tonic and mediated by NMDA receptors and the other third is ramp-like phasic and mediated by non-NMDA receptors. Cholinergic receptors do not appear to be involved. The silent expiratory phase is produced by phasic inhibition of the tonic activity, and ≃80% of this inhibition is mediated by γ-aminobutyric acid receptors (GABA(A)) and ≃20% by glycine receptors. Phasic I inhibition by the I decrementing neurons does not appear to contribute to the predominantly step-ramp patterns of these I neurons. However, this decrementing inhibition may be very prominent in controlling the rate of augmentation in late-onset I neurons and those with ramp patterns lacking the step component.
AB - The relative contribution of phasic and tonic excitatory synaptic drives to the augmenting discharge patterns of inspiratory (I) neurons within the ventral respiratory group (VRG) was studied in anesthetized, ventilated, paralyzed, and vagotomized dogs. Multibarrel micropipettes were used to record simultaneously single-unit neuronal activity and pressure micro-ejected antagonists of GABAergic, glycinergic, N-methyl-D-aspartate (NMDA) and non-NMDA glutamatergic, and cholinergic receptors. The discharge patterns were quantified via cycle-trigger histograms. The findings suggest that two-thirds of the excitatory drive to caudal VRG I neurons is tonic and mediated by NMDA receptors and the other third is ramp-like phasic and mediated by non-NMDA receptors. Cholinergic receptors do not appear to be involved. The silent expiratory phase is produced by phasic inhibition of the tonic activity, and ≃80% of this inhibition is mediated by γ-aminobutyric acid receptors (GABA(A)) and ≃20% by glycine receptors. Phasic I inhibition by the I decrementing neurons does not appear to contribute to the predominantly step-ramp patterns of these I neurons. However, this decrementing inhibition may be very prominent in controlling the rate of augmentation in late-onset I neurons and those with ramp patterns lacking the step component.
KW - Central pattern generation
KW - Control of breathing
KW - Glutamatergic receptors
KW - Neurotransmitters
KW - γ-Aminobutyric acid receptors
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U2 - 10.1152/ajpregu.2000.279.2.r639
DO - 10.1152/ajpregu.2000.279.2.r639
M3 - Article
C2 - 10938255
AN - SCOPUS:0033859199
SN - 0363-6119
VL - 279
SP - R639-R649
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2 48-2
ER -