Journal
BIOCHEMISTRY MOSCOW SUPPLEMENT SERIES A-MEMBRANE AND CELL BIOLOGY
Volume 17, Issue 1, Pages 34-42Publisher
PLEIADES PUBLISHING INC
DOI: 10.1134/S1990747822060058
Keywords
dopamine; glutamate; calcium; excitotoxicity; ionotropic glutamate receptors; neuroprotection
Categories
Ask authors/readers for more resources
Parkinson's disease is characterized by neuronal loss in the midbrain and dopamine-deficient states. It was hypothesized that dopamine may act as a glutamate antagonist and dopamine deficiency may increase glutamate-induced excitotoxicity. Through experiments on rat hippocampal primary culture, dopamine was found to reduce calcium response from NMDA receptors but not from AMPA and KA receptors or voltage-gated calcium channels. The protective effect of dopamine against glutamate toxicity was observed through the reduction of glutamate-induced mitochondrial depolarization and improvement of neuronal survival.
-Parkinson's disease is associated with neuronal loss in the midbrain and the resulting development of dopamine-deficient states. At the later stages of the disease, increased neuronal death is also observed in other parts of the brain. We hypothesized that dopamine may function as a glutamate antagonist, and dopamine deficiency may increase glutamate-induced excitotoxicity. Using rat hippocampal primary culture and fluorescence microscopy, we show that dopamine reduces the amplitude of calcium response evoked by the activation of NMDA receptors but does not affect calcium signals mediated by AMPA and KA receptors. Voltage-gated calcium channels are also unaffected by dopamine. It was shown that the effect of dopamine depends not only on NMDA receptors, but also on D2-type dopamine receptors and on GABA(A) receptor. Dopamine reduced glutamate-induced mitochondrial depolarization and improved neuronal survival in the presence of toxic levels of glutamate. The data presented suggest a protective role of dopamine against glutamate toxicity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available