Gaba sub(B receptors activation in the NTS blocks the glycemic responses induced by carotid body receptor stimulation)

• Published in: Autonomic neuroscience Vol. 141; no. 1-2; pp. 73 - 82
• Main Authors: Lemus, Monica, Montero, Sergio, Cadenas, Jose Luis, Lara, Jose Jesus, Tejeda-Chavez, Hector Rafael, Alvarez-Buylla, Ramon, De Alvarez-Buylla, Elena Roces
• Format: Journal Article
• Language: English
• Published: 18.08.2008
• Subjects: Antagonists; Autonomic nervous system; Baclofen; Bicuculline; Blood; Brain; Carotid body; Chemoreception; Drugs; gamma -Aminobutyric acid A receptors; gamma -Aminobutyric acid B receptors; Glucose; Hyperglycemia; Information processing; Microinjection; Muscimol; Nervous system; Reflexes; Solitary tract nucleus
• ISSN: 1566-0702
• DOI: 10.1016/j.autneu.2008.05.009

The carotid body receptors participate in glucose regulation sensing glucose levels in blood entering the cephalic circulation. The carotid body receptors information, is initially processed within the nucleus tractus solitarius (NTS) and elicits changes in circulating glucose and brain glucose uptake. Previous work has shown that gamma -aminobutyric acid (GABA) in NTS modulates respiratory reflexes, but the role of GABA within NTS in glucose regulation remains unknown. Here we show that GABA sub(B receptor agonist (baclofen) or antagonists (phaclofen and CGP55845A) locally injected into NTS modified arterial glucose levels and brain glucose retention. Control injections outside NTS did not elicit these responses. In contrast, GABA) sub(A) agonist and antagonist (muscimol or bicuculline) produced no significant changes in blood glucose levels. When these GABAergic drugs were applied before carotid body receptors stimulation, again, only GABA sub(B agonist or antagonist significantly affected glycemic responses; baclofen microinjection significantly reduced the hyperglycemic response and brain glucose retention observed after carotid body receptors stimulation, while phaclofen produced the opposite effect, increasing significantly hyperglycemia and brain glucose retention. These results indicate that activation of GABA) sub(B), but not GABA sub(A, receptors in the NTS modulates the glycemic responses after anoxic stimulation of the carotid body receptors, and suggest the presence of a tonic inhibitory mechanism in the NTS to avoid hyperglycemia.)