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Dextrorphan and dextromethorphan attenuate glutamate neurotoxicity.
Brain Research
|February 17, 1987
Summary
Dextrorphan and dextromethorphan were found to reduce glutamate excitotoxicity in mouse brain cells. This suggests these opioids may offer therapeutic benefits for neurological diseases involving neuronal loss.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Glutamate neurotoxicity is implicated in the pathogenesis of neuronal loss in neurological diseases.
- N-methyl-D-aspartate (NMDA) receptor overactivation contributes to excitotoxicity.
- Dextrorphan, a dextrorotatory morphinan opioid, has shown potential in modulating neuronal excitation.
Purpose of the Study:
- To investigate the neuroprotective effects of dextrorphan and its derivative, dextromethorphan, against glutamate-induced neurotoxicity.
- To evaluate the potential therapeutic utility of these compounds in neurological disorders.
Main Methods:
- Murine neocortical cell cultures were utilized.
- Cells were exposed to glutamate to induce neurotoxicity.
- Morphological and chemical evidence of neurotoxicity was assessed.
- The effects of dextrorphan and dextromethorphan (10-100 microM) were evaluated.
Main Results:
- Dextrorphan significantly attenuated both morphological and chemical indicators of glutamate neurotoxicity.
- Dextromethorphan, a methyl ester derivative, demonstrated a similar protective effect.
- The observed neuroprotection occurred at concentrations of 10-100 microM.
Conclusions:
- Dextrorphan and dextromethorphan exhibit neuroprotective properties against glutamate excitotoxicity in vitro.
- These findings suggest a potential therapeutic role for these opioids in managing neurological diseases characterized by neuronal loss.
- Further clinical investigation into dextrorphan, dextromethorphan, and related compounds is warranted.