Experimental petit mal-like seizure induced by microinjection of kainic acid into the unilateral mediodorsal nucleus of the thalamus.
The mediodorsal nucleus (MD) of the thalamus has reciprocal projections with the frontal cortex and limbic system, and may be involved in absence seizures. Kainic acid was injected into the left MD of Wistar rats, and behavior and electroencephalography were monitored for 24 hours, then continued intermittently for 8 weeks. The rat brains were then examined histologically. Brain metabolic changes were also investigated by intravenous injection of 100 microCi/kg of [(14)C]2-deoxyglucose to measure local cerebral glucose metabolism. Bilateral synchronous spike and wave complexes appeared almost 2 hours after kainic acid injection, and the waveforms continued for about 5-7 hours in the bilateral MDs, ipsilateral sensorimotor cortex, and basolateral nucleus of the amygdala. The associated behavioral changes were mainly those of behavioral arrest and staring, associated with occasional limbic seizures. Clear metabolic increases were found in the ipsilateral frontal cortex, hippocampus, and amygdala. The present results suggest that the MD was involved in both the mechanism of spike and wave complexes in the bilateral frontal cortices, and in seizure propagation to the limbic system. Consequently, kainic acid-induced MD seizure is associated with significant cognitive impairment and may explain the mechanism of petit mal seizure.
Kato
Koichi
K
Department of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan. kkato@nij.twmu.ac.jp
Urino
Tomoyuki
T
Hori
Tomokatsu
T
Tsuda
Hiroshige
H
Yoshida
Katsunari
K
Hashizume
Kiyotaka
K
Tanaka
Tatsuya
T
D000679:Amygdala / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001364:Awareness / Q000187:drug effects / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D004195:Disease Models, Animal; D004292:Dominance, Cerebral / Q000502:physiology; D004569:Electroencephalography / Q000187:drug effects; D004832:Epilepsy, Absence / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D005071:Evoked Potentials / Q000187:drug effects; D005625:Frontal Lobe / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D007608:Kainic Acid / Q000633:toxicity; D008297:Male; D020645:Mediodorsal Thalamic Nucleus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009044:Motor Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D009048:Motor Skills / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D013239:Stereotyped Behavior / Q000187:drug effects / Q000502:physiology
D001786:Blood Glucose; D007608:Kainic Acid