Hindbrain cytoglucopenia-induced increases in systemic blood glucose levels by 2-deoxyglucose depend on intact astrocytes and adenosine release

The hindbrain contains critical neurocircuitry responsible for generating defensive physiological responses to hypoglycemia. This counter-regulatory response (CRR) is evoked by local hindbrain cytoglucopenia that causes an autonomically mediated increase in blood glucose, feeding behavior, and accel...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2016-06, Vol.310 (11), p.R1102-R1108
Main Authors: Rogers, Richard C, Ritter, Sue, Hermann, Gerlinda E
Format: Article
Language:English
Subjects:
Adenosine - metabolism
Animals
Astrocytes - drug effects
Astrocytes - metabolism
Blood Glucose - drug effects
Blood Glucose - metabolism
Deoxyglucose - administration & dosage
Female
Glucose
Homeostasis
Homeostasis - drug effects
Hypoglycemia
Hypoglycemia - metabolism
Infusions, Intraventricular
Male
Medical research
Neural Control
Neurology
Obesity, Diabetes and Energy Homeostasis
Rats
Rats, Long-Evans
Rhombencephalon - metabolism
Rhombencephalon - pathology
Up-Regulation - drug effects
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The hindbrain contains critical neurocircuitry responsible for generating defensive physiological responses to hypoglycemia. This counter-regulatory response (CRR) is evoked by local hindbrain cytoglucopenia that causes an autonomically mediated increase in blood glucose, feeding behavior, and accelerated digestion; that is, actions that restore glucose homeostasis. Recent reports suggest that CRR may be initially triggered by astrocytes in the hindbrain. The present studies in thiobutabarbital-anesthetized rats show that exposure of the fourth ventricle (4V) to 2-deoxyglucose (2DG; 15 μmol) produced a 35% increase in circulating glucose relative to baseline levels. While the 4V application of the astrocytic signal blocker, fluorocitrate (FC; 5 nmol), alone, had no effect on blood glucose levels, 2DG-induced increases in glucose were blocked by 4V FC. The 4V effect of 2DG to increase glycemia was also blocked by the pretreatment with caffeine (nonselective adenosine antagonist) or a potent adenosine A1 antagonist (8-cyclopentyl-1,3-dipropylxanthine; DPCPX) but not the NMDA antagonist (MK-801). These results suggest that CNS detection of glucopenia is mediated by astrocytes and that astrocytic release of adenosine that occurs after hypoglycemia may cause the activation of downstream neural circuits that drive CRR.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00493.2015