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Toxic effect of lithium in mouse brain.
1Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis 55455.
Summary
High lithium concentrations inhibit glucose oxidation in mouse brains, while chronic administration reduces DNA content. Glucose utilization in the cerebrum increases significantly during postnatal development, unlike the cerebellum.
Area of Science:
- Neuroscience
- Biochemistry
- Developmental Biology
Background:
- Lithium is a mood stabilizer with known neurological effects.
- Understanding lithium's impact on brain metabolism and development is crucial.
- Glucose oxidation is a key indicator of brain energy metabolism.
Purpose of the Study:
- To investigate the in vitro effects of lithium on glucose oxidation in mouse cerebrum and cerebellum.
- To assess the impact of chronic lithium administration on brain DNA content.
- To examine the developmental changes in glucose utilization in the postnatal brain.
Main Methods:
- In vitro measurement of isotopic glucose conversion to 14CO2/mg wet weight.
- Chronic lithium administration to adult mice.
- Measurement of DNA content in postnatal cerebrum and cerebellum.
Main Results:
- High lithium concentrations (197-295 mM) inhibited glucose oxidation.
- Chronic lithium (80-108 mM) decreased cerebrum and cerebellum DNA content.
- Cerebral glucose utilization increased significantly from postnatal Day 1 to Day 20, reaching adult levels.
- Cerebellar glucose oxidation remained constant during postnatal growth.
Conclusions:
- Lithium's effect on glucose oxidation is dose-dependent.
- Chronic lithium affects brain DNA content, particularly during development.
- The cerebrum shows marked developmental changes in glucose utilization, while the cerebellum remains relatively stable.
