5-Hydroxytryptamine attenuates free radical injury in primary mouse cortical cultures.

Abstract

The effects of 5-hydroxytryptamine (5-HT) on several types of neuronal injury in mouse cortical cell cultures were tested. Co-treatment with 5-HT prevented free radical-mediated neuronal necrosis induced by FeCl2 or buthionine sulfoximine (BSO) in a dose-dependent manner. Subtype antagonists did not reverse the protective effect and 5-HT showed direct free radical scavenging activity evidenced by its ability to reduce the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) in a cell-free system. Excitotoxic necrosis induced by NMDA or apoptosis induced by staurosporine was not sensitive to 5-HT treatment. These features raise the possibility that the endogenous neurotransmitter 5-HT may work as an innate antioxidant defense mechanism in the CNS.

• Authors: J Y Kang, H J Kang, Y K Chung, B J Gwag, J S Noh
• Journal: Neuroreport (Neuroreport) Vol. 12 Issue 5 Pg. 963-6 (Apr 17 2001) ISSN: 0959-4965 [Print] England
• PMID: 11303769 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antioxidants
• Free Radical Scavengers
• Free Radicals
• Neuroprotective Agents
• Serotonin Antagonists
• Serotonin
• Staurosporine

Topics

• Animals
• Antioxidants (pharmacology)
• Apoptosis (drug effects)
• Cell Death (drug effects)
• Cells, Cultured
• Cerebral Cortex (pathology)
• Free Radical Scavengers (pharmacology)
• Free Radicals (toxicity)
• Mice
• Neurons (drug effects)
• Neuroprotective Agents (pharmacology)
• Serotonin (pharmacology)
• Serotonin Antagonists (pharmacology)
• Staurosporine (toxicity)