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Published on: April 11, 2018
Taurine release in mouse brain stem slices under cell-damaging conditions
1Tampere Brain Research Center, Medical School, University of Tampere, and Centre for Laboratory Medicine, Tampere University Hospital, Finland. blpisa@uta.fi
Amino Acids
|September 26, 2006
Summary
Taurine release significantly increases in the brain stem during damaging conditions like ischemia, except with free radicals. This release, mediated by transporters and ion channels, may protect neural cells from excitotoxicity.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Taurine is vital for neural cell development, survival, and protection.
- The brain stem relies on taurine for regulating critical functions like blood pressure.
- Previous studies characterized normal taurine release; this study investigates release under stress.
Purpose of the Study:
- To investigate [3H]taurine release from mouse brain stem slices under various cell-damaging conditions.
- To compare taurine release in developing versus adult mice.
- To elucidate the mechanisms underlying ischemia-induced taurine release.
Main Methods:
- Superfusion system used to study preloaded [3H]taurine release.
- Mouse brain stem slices from 7-day-old and 3-month-old mice were used.
- Conditions included hypoxia, hypoglycemia, ischemia, metabolic poisons, and free radicals.
Main Results:
- Taurine release was enhanced under hypoxia, hypoglycemia, ischemia, and metabolic poisons, but not free radicals.
- Ischemia-induced release involved both Ca2+-dependent and -independent pathways.
- Release was mediated by Na+-, Cl--dependent transporters and Cl- channels, particularly in immature brain stems.
- Protein kinase C, cyclic GMP, and phospholipases were implicated in the release mechanisms.
Conclusions:
- Taurine release is significantly upregulated in the brain stem under various cell-damaging conditions.
- Ischemia-induced taurine release involves complex transport and signaling pathways.
- This release mechanism may serve a protective role against excitotoxicity in the brain stem.
