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Nitric oxide modulates dopamine release during global temporary cerebral ischemia
R A Kahn1, J Weinberger, T Brannan
1Department of Anesthesiology, Mount Sinai Medical Center, New York, NY 10029, USA.
Anesthesia and Analgesia
|June 1, 1995
Summary
Nitric oxide (NO) mediates dopamine (DA) release during cerebral ischemia. Inhibiting NO synthase with L-NAME significantly reduced ischemic DA release, suggesting NO
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Dopamine (DA) is released in the striatum during cerebral ischemia.
- DA contributes to neuronal injury alongside excitatory neurotransmitters.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in ischemia-induced DA release.
- To determine if NO modulates DA release during cerebral ischemia.
Main Methods:
- Used Sprague-Dawley rats with microdialysis probes in the corpus striatum.
- Administered L-NAME (a NO synthase inhibitor) or vehicle.
- Induced temporary global forebrain ischemia via carotid artery ligation and hypotension.
Main Results:
- L-NAME administration reduced ischemic extraneuronal DA concentration by 60%.
- DOPAC and HVA concentrations increased during recovery in controls.
- L-NAME reduced HVA concentration during recovery compared to vehicle.
Conclusions:
- Ischemic dopamine release appears to be mediated by nitric oxide (NO).
- NO-modulated DA release may contribute to NO's neurotoxic effects during ischemia.