Abstract
The authors examined the role of nitric oxide (NO) in the relationship between kainate-induced neuronal death and locomotion changes. Locomotion was significantly increased 1 h after kainate injection, suggesting that kainate induced NO and dopamine release. Cell death occurred in the CA1 (41%) and CA3 (54%) regions at 12 h. At 7 days, GABAergic neurons in striatum were lost, suggesting possible pyramidal neuron synapse with striatal GABAergic neurons, and pyramidal neuron damage leading to deafferentation and degeneration of striatal GABAergic neurons. Pre-administration of Nw-nitro-L-arginine-methyl-ester or 7-nitroindazole reduced these effects. These results indicate that NO may modulate kainate-induced neuronal death and locomotion.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Death / drug effects
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Denervation
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Enzyme Inhibitors / pharmacology
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Excitatory Amino Acid Agonists
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / pathology*
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Indazoles / pharmacology
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Kainic Acid
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Motor Activity / drug effects
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Motor Activity / physiology*
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NG-Nitroarginine Methyl Ester / pharmacology
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Neostriatum / metabolism
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Neostriatum / pathology*
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Neural Pathways
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Nitric Oxide / metabolism*
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Pyramidal Cells / metabolism
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Pyramidal Cells / pathology*
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Rats
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Rats, Sprague-Dawley
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gamma-Aminobutyric Acid / metabolism*
Substances
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Enzyme Inhibitors
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Excitatory Amino Acid Agonists
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Indazoles
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Nitric Oxide
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gamma-Aminobutyric Acid
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Kainic Acid
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7-nitroindazole
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NG-Nitroarginine Methyl Ester