nervous system
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• following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), seizures are more frequent and last longer than in similarly treated wild-type mice
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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• dorsal columns lack myelin unlike in wild-type mice
• mice exhibit amyelinated and hypomyelinated axons unlike in wild-type mice
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• mice exhibit amyelinated and hypomyelinated axons unlike in wild-type mice
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behavior/neurological
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• following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), seizures are more frequent and last longer than in similarly treated wild-type mice
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• on a rotarod at baseline and after treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)
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• hindlimb and tail paresis following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)
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homeostasis/metabolism
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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cellular
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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