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Updated: May 13, 2026
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Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
Published on: March 11, 2020
Striatal glutamate degenerates thalamic neurons
Ingrid Morales1, Catalina Yanos, Clara Rodriguez-Sabate
1Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, Faculty of Medicine, University of La Laguna, La Laguna, Tenerife, Canary Islands.
Journal of Neuropathology and Experimental Neurology
|March 14, 2013
Summary
Excessive glutamate (GLU) can cause brain cell damage. This study shows that brain injury can trigger self-induced GLU accumulation in astrocytes, contributing to neurodegeneration in basal ganglia disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Glutamate (GLU)-induced excitotoxicity is a known cause of cell degeneration in basal ganglia disorders.
- Astrocytes normally prevent excitotoxicity by taking up GLU.
- Recent findings suggest GLU perfusion in the striatum causes persistent GLU accumulation in astrocytes.
Purpose of the Study:
- To investigate the induction of self-induced GLU accumulation (SIGA) after injury.
- To determine if SIGA occurs following GLU receptor agonist perfusion in the rat striatum.
Main Methods:
- Perfusion of GLU receptor agonists into the striatum of rats.
- Histological analysis to assess neuronal and axonal degeneration, microgliosis, and astrocytosis.
- Examination of GLU accumulation in astrocytes in both local (striatum) and remote (thalamus) brain regions.
Main Results:
- GLU receptor agonists induced local neuronal and axonal degeneration, microgliosis, and astrocytosis.
- Gliosis and remote neuronal degeneration were observed in the thalamus.
- Persistent GLU accumulation in reactive astrocytes (local and remote SIGA) was detected for at least 6 weeks post-injury.
Conclusions:
- Neuronal degeneration can retrogradely trigger SIGA via excessive endogenous GLU release from astrocytes.
- SIGA may be a significant factor in basal ganglia disorders characterized by glutamatergic excitotoxicity.
- This mechanism highlights a novel pathway contributing to neurodegeneration in brain injury.
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