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Published on: December 19, 2019
Substantia nigra osmoregulation: taurine and ATP involvement
Ingrid Morales1, Jose G Dopico, Magdalena Sabate
1Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, Faculty of Medicine, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain.
Glial cells in the substantia nigra release taurine in response to osmotic changes. This osmoregulation involves glutamate and ATP, potentially impacting Parkinson's disease.
Area of Science:
- Neuroscience
- Glial Biology
- Neurochemistry
Background:
- A glial-derived extracellular taurine pool exists in the substantia nigra (SN).
- Taurine's inhibitory role in the SN is known, but the function of this nonsynaptic pool is unexplored.
Purpose of the Study:
- To investigate the physiological role of the nonsynaptic taurine pool in the rat SN.
- To explore the influence of local osmolarity on this taurine pool.
Main Methods:
- Microdialysis techniques were employed in the rat SN.
- Local osmolarity was manipulated using hypoosmolar and hyperosmolar pulses.
- The effects of glutamate receptor antagonists (6-cyano-7-nitroquinoxaline-2,3-dionine disodium) and purinergic receptor antagonists (pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid) were assessed.
- Adenosine triphosphate (ATP) was administered to study purinergic receptor involvement.
Main Results:
- Hypoosmolar pulses increased extrasynaptic taurine in the SN dose-dependently.
- Hyperosmolar pulses decreased extrasynaptic taurine.
- Blockade of AMPA-kainate glutamate receptors and purinergic receptors altered basal taurine levels.
- These receptor antagonists also diminished the taurine response to hypoosmolar stimuli.
- ATP administration modulated basal taurine levels and the response to hypoosmolarity.
Conclusions:
- The nonsynaptic taurine pool in the SN appears to play a role in osmoregulation.
- Glutamatergic and purinergic signaling are involved in mediating the taurine response to osmotic changes.
- This osmoregulatory function may influence neuronal vulnerability in conditions like Parkinson's disease.
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