Related Experiment Video
Updated: Jun 27, 2026

05:49
Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
Published on: May 5, 2021
High glucose changes extracellular adenosine triphosphate levels in rat retinal cultures
1Center for Neuroscience and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Journal of Neuroscience Research
|December 17, 2008
Summary
High glucose levels in diabetes increase extracellular adenosine triphosphate (ATP) release in the retina, potentially driving inflammation and diabetic retinopathy (DR). This study reveals altered purinergic signaling in high-glucose conditions.
Area of Science:
- Ophthalmology
- Neuroscience
- Cell Biology
Background:
- Diabetic retinopathy (DR) is a leading cause of adult blindness.
- Diabetes triggers retinal inflammation via microglial activation and inflammatory mediators.
- The precise mechanism linking diabetes to retinal inflammation remains unclear.
Purpose of the Study:
- To investigate the effect of high glucose on extracellular adenosine triphosphate (ATP) levels in retinal cell cultures.
- To explore the role of purinergic signaling in high-glucose-induced retinal inflammation.
Main Methods:
- Cultured retinal cells exposed to high glucose (hyperglycemia model).
- Measured extracellular ATP levels following depolarizing stimuli.
- Assessed ATP degradation and intracellular calcium concentrations.
- Utilized botulinum neurotoxin A and calcium removal to investigate mechanisms.
Main Results:
- High glucose significantly increased extracellular ATP release after stimulation.
- ATP elevation was dependent on extracellular calcium and sensitive to botulinum neurotoxin A.
- Degradation of extracellular ATP was reduced in high-glucose conditions.
- High glucose enhanced intracellular calcium concentration changes.
Conclusions:
- High glucose disrupts the retinal purinergic system by increasing ATP exocytosis and reducing degradation.
- Elevated extracellular ATP in diabetic retinas may promote inflammation contributing to DR pathogenesis.

