Prior results from this laboratory have demonstrated that the respiratory response to
hypercapnia is enhanced by microinjection of
GABA antagonists or
GABA synthesis inhibitors into the caudal hypothalamus of both cats and rats. However, no evidence was found for modulation of the respiratory response to
hypoxia by a hypothalamic GABAergic mechanism. The purpose of the present study was to determine if synaptic input other than GABAergic onto caudal hypothalamic neurons affects the respiratory responses to
hypoxia. The respiratory (diaphragmatic EMG) responses to
hypoxia (10% O2) and
hypercapnia (5% CO2) were recorded in anesthetized rats before and after bilateral microinjection of a blocker of synaptic transmission (CoCl2, 100 mM) or an
excitatory amino acid receptor antagonist (
kynurenic acid, 50 mM) into the caudal hypothalamus. Both
hypoxia and
hypercapnia elicited increases in tidal diaphragmatic activity and respiratory frequency prior to the microinjections. The respiratory response to
hypercapnia was increased (+10.5%) after CoCl2 microinjections, which is consistent with prior results obtained with blockade of GABAergic input.
Kynurenic acid did not alter the respiratory response to
hypercapnia. A new finding was that the respiratory response to
hypoxia was diminished after both CoCl2 (-13.0%) and
kynurenic acid (-25.0%) microinjections. The results of this study support our prior findings that neurons in the caudal hypothalamus modulate the respiratory response to
hypercapnia. In addition, our findings suggest that an excitatory input acting through
excitatory amino acid receptors in the caudal hypothalamus modulates the respiratory responses to
hypoxia.