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Protective action of dopamine against glutamate neurotoxicity in the retina.
Invest Ophthalmol Vis Sci. 1994 Feb; 35(2):685-95.IO

Abstract

PURPOSE

The electrophysiologic study using patch-clamp techniques demonstrated that NMDA-induced currents had properties similar to those recorded in the brain.

METHODS

Primary cultures obtained from the fetal rat retina (gestation days 16 to 19) were used for the experiment. Immunocytochemical and electrophysiologic studies were done to identify the cultured cells. The neurotoxic effects of glutamate or N-methyl-D-aspartate (NMDA) on the retinal cultures were quantitatively assessed using the trypan blue exclusion method.

RESULTS

The immunocytochemical study revealed that the major component of the rat retinal cultures was neurons including amacrine cells. The electrophysiologic study using patch-clamp techniques demonstrated that exposure to NMDA-induced currents with properties characteristic of those recorded in the brain. Brief exposure of these neurons to glutamate or NMDA induced delayed cell death. Glutamate neurotoxicity was prevented by the application of dopamine and forskolin. The protective action of dopamine was antagonized by a D1 receptor antagonist (SCH 23390) but not by D2 receptor antagonists (domperidone and sulpiride). A D1 receptor agonist (SKF 38393) protected glutamate-induced neurotoxicity in a concentration-dependent manner, whereas a D2 receptor agonist (quinpirole) did not affect it.

CONCLUSIONS

These findings demonstrate that dopamine protects retinal neuronal cells against NMDA receptor-mediated glutamate neurotoxicity via D1 receptors.

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Authors+Show Affiliations

Kashii S
Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
Takahashi M
No affiliation info available
Mandai M
No affiliation info available
Shimizu H
No affiliation info available
Honda Y
No affiliation info available
Sasa M
No affiliation info available
Ujihara H
No affiliation info available
Tamura Y
No affiliation info available
Yokota T
No affiliation info available
Akaike A
No affiliation info available

MeSH

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineAnimalsBenzazepinesCell DeathCells, CulturedDopamineDopamine AntagonistsDose-Response Relationship, DrugElectrophysiologyExcitatory Amino Acid AntagonistsFetusFluorescent Antibody TechniqueGlutamatesGlutamic AcidN-MethylaspartateNerve Tissue ProteinsNeuronsRatsReceptors, N-Methyl-D-AspartateRetina

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7906683

Citation

Kashii, S, et al. "Protective Action of Dopamine Against Glutamate Neurotoxicity in the Retina." Investigative Ophthalmology & Visual Science, vol. 35, no. 2, 1994, pp. 685-95.
Kashii S, Takahashi M, Mandai M, et al. Protective action of dopamine against glutamate neurotoxicity in the retina. Invest Ophthalmol Vis Sci. 1994;35(2):685-95.
Kashii, S., Takahashi, M., Mandai, M., Shimizu, H., Honda, Y., Sasa, M., Ujihara, H., Tamura, Y., Yokota, T., & Akaike, A. (1994). Protective action of dopamine against glutamate neurotoxicity in the retina. Investigative Ophthalmology & Visual Science, 35(2), 685-95.
Kashii S, et al. Protective Action of Dopamine Against Glutamate Neurotoxicity in the Retina. Invest Ophthalmol Vis Sci. 1994;35(2):685-95. PubMed PMID: 7906683.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective action of dopamine against glutamate neurotoxicity in the retina. AU - Kashii,S, AU - Takahashi,M, AU - Mandai,M, AU - Shimizu,H, AU - Honda,Y, AU - Sasa,M, AU - Ujihara,H, AU - Tamura,Y, AU - Yokota,T, AU - Akaike,A, PY - 1994/2/1/pubmed PY - 1994/2/1/medline PY - 1994/2/1/entrez SP - 685 EP - 95 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 35 IS - 2 N2 - PURPOSE: The electrophysiologic study using patch-clamp techniques demonstrated that NMDA-induced currents had properties similar to those recorded in the brain. METHODS: Primary cultures obtained from the fetal rat retina (gestation days 16 to 19) were used for the experiment. Immunocytochemical and electrophysiologic studies were done to identify the cultured cells. The neurotoxic effects of glutamate or N-methyl-D-aspartate (NMDA) on the retinal cultures were quantitatively assessed using the trypan blue exclusion method. RESULTS: The immunocytochemical study revealed that the major component of the rat retinal cultures was neurons including amacrine cells. The electrophysiologic study using patch-clamp techniques demonstrated that exposure to NMDA-induced currents with properties characteristic of those recorded in the brain. Brief exposure of these neurons to glutamate or NMDA induced delayed cell death. Glutamate neurotoxicity was prevented by the application of dopamine and forskolin. The protective action of dopamine was antagonized by a D1 receptor antagonist (SCH 23390) but not by D2 receptor antagonists (domperidone and sulpiride). A D1 receptor agonist (SKF 38393) protected glutamate-induced neurotoxicity in a concentration-dependent manner, whereas a D2 receptor agonist (quinpirole) did not affect it. CONCLUSIONS: These findings demonstrate that dopamine protects retinal neuronal cells against NMDA receptor-mediated glutamate neurotoxicity via D1 receptors. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/7906683/Protective_action_of_dopamine_against_glutamate_neurotoxicity_in_the_retina_ L2 - https://iovs.arvojournals.org/article.aspx?volume=35&issue=2&page=685 DB - PRIME DP - Unbound Medicine ER -