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Behavioral Assessment of Visual Function via Optomotor Response and Cognitive Function via Y-Maze in Diabetic Rats
Published on: October 23, 2020
Cognitive dysfunction associated with diabetic ketoacidosis in rats
Nicole Glaser1, Steve Anderson, Wesley Leong
1Department of Pediatrics, University of California Davis, School of Medicine, Sacramento, CA 95817, USA. nsglaser@ucdavis.edu
Neuroscience Letters
|January 24, 2012
Summary
A single episode of diabetic ketoacidosis (DKA) in juvenile rats impaired learning abilities. This finding in our animal model supports concerns that DKA may cause cognitive deficits in children with type 1 diabetes.
Area of Science:
- Neuroscience
- Endocrinology
- Pediatrics
Background:
- Type 1 diabetes mellitus (T1DM) in children is linked to neurocognitive deficits.
- Diabetic ketoacidosis (DKA) may be associated with memory impairment in pediatric T1DM.
- The cause of these potential neurocognitive deficits remains unclear.
Purpose of the Study:
- To investigate if a single episode of DKA causes cognitive deficits.
- To establish an animal model for studying DKA-induced neurocognitive effects.
- To determine if DKA impacts learning and memory in juvenile rats.
Main Methods:
- Diabetes was induced in juvenile rats using streptozotocin.
- One group developed DKA via insulin withdrawal, followed by treatment.
- Cognitive function was assessed using the Morris Water Maze post-DKA recovery.
Main Results:
- Rats experiencing DKA showed significantly longer latency times in the Morris Water Maze.
- Delayed learning was observed in the DKA group compared to diabetic controls.
- These differences were evident on days 7 and 8 of cognitive testing.
Conclusions:
- A single DKA episode leads to measurable learning deficits in rats.
- These findings align with potential DKA-related neurocognitive issues in children with T1DM.
- DKA may be a contributing factor to cognitive impairments in pediatric type 1 diabetes.
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