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First Department of Internal Medicine, Tohoku University School of Medicine, Sendai 980-8574, Japan
The purpose of this
study was to examine our hypothesis that 
-aminobutyric acid
(GABA) in the nucleus tractus solitarii (NTS) may be related to the
hypoxic ventilatory decline (HVD) and that chemoreceptor stimulation
was essential to activate this mechanism. We used unanesthetized,
freely moving rats in this study. An in vivo microdialysis technique
was used to measure the extracellular GABA concentration
([GABA]o), and an in vivo microinjection technique was
used to examine the effects of the GABA agonists and antagonists on the
ventilation during hypoxia. The GABA agonists injected into the NTS
attenuated the ventilation during hypoxia. By hypoxic exposure,
[GABA]o was increased during the HVD. However, by carotid body denervation (CBD), this GABA increase was abolished. Although GABA
antagonists microinjected into the NTS during the HVD phase significantly increased the depressed ventilation, this effect on the
ventilation was abolished by CBD. These results suggest that the GABA
in the NTS has a pivotal role in the HVD and that this mechanism is not
activated without chemoreceptor stimulation.
hypoxia; -aminobutyric acid receptor; microdialysis; carotid
body denervation; control of breathing
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