Astrocytes are glial cells in central nervous system, ideally positioned to uptake glucose from the blood and to support surrounding neurons with metabolites, such as L-lactate. Astrocytes produce L-lactate in the process of aerobic glycolysis where glucose derives from glycogen degradation. Glycogen degrades after adrenergic stimulation into final product L-lactate, which may support surrounding neurons. In this work we showed that all L-lactate after adrenergic stimulation derives from glycogen, and that Krebs cycle is the main metabolic pathway in astrocytes at rest. Astrocytes express many GPCRs, including cannabinoid receptors CB1 and CB2. Activation of cannabinoid receptors with agonists stimulated exocytosis, measured with the whole-cell patch clamp membrane capacitance measurements. CB2R stimulation affected D-glucose and L-lactate metabolism, whereas CB1R only transiently increased L-lactate and glucose concentration. Stimulation of CB1 or CB2 receptors has no effect on the volume of cells at the hypoosmolar challenge. We conclude that cannabinoid signalling system affects astrocyte metabolism, stimulates exocytosis, but has no effect on the swelling of cells after hypoosmolar shock.
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