Hypothalamic GABAergic mechanism involved in respiratory response to hypercapnia.
Previous studies have demonstrated that suprapontine areas of the brain modulate the respiratory responses to hypoxia and hypercapnia. The purpose of the present study was to determine if neurons in the posterior hypothalamus are responsible for this modulation. The respiratory (monitored from diaphragmatic activity) and cardiovascular responses to hypoxia and to hypercapnia were examined in anesthetized rats before and after microinjection of a GABA synthesis inhibitor (3-mercaptopropionic acid, 3-MP) into the posterior hypothalamus. Unilateral micro-injection of 3-MP into the posterior hypothalamus elicited an increase in minute diaphragmatic activity (+54.9 +/- 15.8%), arterial pressure (10.5 +/- 3.2 mmHg) and heart rate (26.8 +/- 10.7 min-1) after a delay of 15-20 minutes. The respiratory responses to hypercapnia but not the cardiovascular responses were greatly accentuated after hypothalamic microinjections of 3-mercaptopropionic acid. In contrast, none of the responses (increases in diaphragmatic activity and heart rate; fall in arterial pressure) elicited by hypoxia were altered after microinjections of the GABA synthesis inhibitor into the posterior hypothalamus. These findings indicate that a GABAergic inhibition of posterior hypothalamic neurons modulates the respiratory response to hypercapnia.[1]References
- Hypothalamic GABAergic mechanism involved in respiratory response to hypercapnia. Peano, C.A., Shonis, C.A., Dillon, G.H., Waldrop, T.G. Brain Res. Bull. (1992) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
