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Sustained limbic seizures induced by intraamygdaloid kainic acid in the baboon: Symptomatology and neuropathological consequences
Author(s) -
Menini Christian,
Meldrum Brian S.,
Riche Danielle,
SilvaComte Carmen,
Stutzmann Jean Marie
Publication year - 1980
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410080507
Subject(s) - kainic acid , status epilepticus , gliosis , hippocampus , neuroscience , hippocampal formation , baboon , neocortex , amygdala , limbic system , epilepsy , psychology , medicine , pathology , central nervous system , glutamate receptor , receptor
In Papio papio baboons chronically prepared for cortical and deep electroencephalographic recording, injection of kainic acid into the amygdala (7 animals) or temporal pole (2 animals) gave rise to focal epileptic discharges lasting 15 to 150 hours. Electrographically, the seizure activity spread ipsilaterally and contralaterally within the limbic system but did not become generalized. The principal associated motor signs were arrest of movement and oral automatisms. Histological examination after two to ten days demonstrated lesions (neuron loss and gliosis) at the injection site that varied according to the amount of kainic acid injected (2 to 68 μg). “Remote” lesions occurred in the ipsilateral hippocampus (end‐folium and Sommer sector) and neocortex (occipital and frontal regions). The hippocampal lesions were comparable to those previously described as consequent to status epilepticus.