Abstract
Dimebon in low concentrations potentiated activity of AMPA-receptors in rat cerebellar Purkinje neurons, while memantine produced only an insignificant potentiation in a small group of these cells. In cortical neurons of rat brain memantine efficiently blocked NMDA-induced currents in dimebon-insensitive neurons. By contrast, its effect was far weaker in neurons, where the blocking action of dimebon on NMDA-receptors was most pronounced. It was hypothesized that the differences in the effects of memantine and dimebon are determined by their interaction with different sites of NMDA-receptors.
MeSH terms
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Animals
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Benzothiadiazines / pharmacology
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism
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Excitatory Amino Acid Agonists / pharmacology
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Excitatory Amino Acid Antagonists / pharmacology*
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Indoles / pharmacology*
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Kainic Acid / pharmacology
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Memantine / pharmacology*
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N-Methylaspartate / pharmacology
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Neurons / drug effects
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Neurons / metabolism*
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Patch-Clamp Techniques
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Purkinje Cells / cytology
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Purkinje Cells / drug effects
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Purkinje Cells / metabolism
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Rats
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Receptors, AMPA / drug effects
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Receptors, AMPA / metabolism*
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / metabolism*
Substances
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Benzothiadiazines
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Excitatory Amino Acid Agonists
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Excitatory Amino Acid Antagonists
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Indoles
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Receptors, AMPA
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Receptors, N-Methyl-D-Aspartate
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N-Methylaspartate
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latrepirdine
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cyclothiazide
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Kainic Acid
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Memantine