mortality/aging
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• within 10 minutes of kainic acid infusion, vigorous status epilepticus leads to death in transgenic animals whereas no wild-type mice die after kainic acid treatment
|
behavior/neurological
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• intensity of kainic acid-induced seizures is elevated in transgenic mice relative to wild-type
|
|
• severe seizures in kainic acid-treated mice are associated with generalized tonic-clonic seizures with wild seizure jumps, while wild-type mice do not show any myoclonic twitches
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nervous system
| N |
• no amyloid beta deposits are observed in transgenic mouse brains
• no differences in neuron number in cingulate cortex relative to wild-type
|
|
• intensity of kainic acid-induced seizures is elevated in transgenic mice relative to wild-type
|
|
• severe seizures in kainic acid-treated mice are associated with generalized tonic-clonic seizures with wild seizure jumps, while wild-type mice do not show any myoclonic twitches
|
|
• PTGS2 overexpression in neurons potentiates amyloid beta-mediated neuronal apoptotic damage in cortico-hippocampal cultures
|
|
• in cultured cortico-hippocampal neurons, exposure to glutamate results in 46% impairment of redox activity compared to 31.2% in control neurons, indicating potentiation of excitotoxicity in vitro
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homeostasis/metabolism
|
• in cultured cortico-hippocampal neurons, exposure to glutamate results in 46% impairment of redox activity compared to 31.2% in control neurons, indicating potentiation of excitotoxicity in vitro
|
cellular
|
• in cultured cortico-hippocampal neurons, exposure to glutamate results in 46% impairment of redox activity compared to 31.2% in control neurons, indicating potentiation of excitotoxicity in vitro
|


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