Related Experiment Videos
Delayed decrease of excitatory amino acid neurotransmitters in parietotemporal cortex and hippocampus after complete
1Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Im Neuenheimer Feld 220-221, 69120 Heidelberg, Germany.
Archives of Gerontology and Geriatrics
|January 1, 1997
Summary
Aged rats subjected to cerebral ischemia showed significant changes in amino acid neurotransmitters (AANT) in the brain. Old rats experienced greater glutamate and aspartate depletion, suggesting heightened vulnerability to ischemic damage.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Amino acid neurotransmitters (AANT) play critical roles in brain function.
- Cerebral ischemia can disrupt neurotransmitter balance and lead to neuronal damage.
- Aging may exacerbate the effects of ischemia on brain tissue.
Purpose of the Study:
- To investigate changes in key AANT levels in aged rats following cerebral ischemia.
- To compare the neurochemical response to ischemia in the hippocampus and parietotemporal cortex.
- To explore the potential link between altered AANT levels and delayed neuronal damage in aged brains.
Main Methods:
- A 15-minute complete cerebral ischemia (CCI) model was employed in aged rats.
- Tissue contents of glutamate, aspartate, GABA, and glycine were measured using High-Performance Liquid Chromatography (HPLC).
- Measurements were taken during ischemia and up to 96 hours of postischemic recirculation.
Main Results:
- Excitatory AANT (glutamate, aspartate) decreased during and after ischemia, with enhanced depletion in aged rats compared to young ones.
- A second decrease in glutamate and aspartate correlated with energy metabolism disturbances, suggesting a role in delayed neuronal damage.
- Reduced GABA in the hippocampus and decreased glycine in the parietotemporal cortex were observed, indicating region-specific vulnerability and potential NMDA receptor dysfunction.
Conclusions:
- Aged rats exhibit an enhanced release and depletion of excitatory AANT following cerebral ischemia.
- Imbalances in inhibitory and excitatory AANT, particularly in the hippocampus, suggest greater vulnerability to ischemic injury in this region.
- Decreased glycine in the parietotemporal cortex may contribute to the higher susceptibility of the hippocampus to ischemic damage in aged individuals.