Long-term observation of rats after unilateral intra-amygdaloid injection of kainic acid

Tanaka, Shigeya; Kondo, Shinji; Tanaka, Tatsuya; Yonemasu, Yukichi

doi:10.1016/0006-8993(88)90541-0

Cited by 59 publications

(33 citation statements)

References 12 publications

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“…1,24) Our study also showed mild neuronal cell loss in the hippocampus, but spontaneous seizures were not observed in the chronic stage. GAERS, which is considered to be the typical absence seizure model, have shown no SWDs in the hippocampus.…”

Section: Discussionsupporting

confidence: 56%

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Kato

Urino

Hori

et al. 2008

Neurol. Med. Chir.(Tokyo)

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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 mCi/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.

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Section: Discussionsupporting

confidence: 56%

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Kato

Urino

Hori

et al. 2008

Neurol. Med. Chir.(Tokyo)

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“…A stainless steel cannula with internal stylet for KA (Nacalai tesque, Kyoto, Japan) microinjection, 0.03 mm in internal diameter, was implanted in the left amygdala using sterile techniques. Coordinates for the implantation target were: AP +5 mm, ML +5 mm and DV +2 mm with respect to the interaural zero point (20). The cannula was fixed with dental cement.…”

Section: Experimental Model For Temporal Lobe Epilepsymentioning

confidence: 99%

“…Kainate (KA) administration, an experimental model for human temporal lobe epilepsy (18), is known to engender abnormal excitation/inhibition in the limbic system (19), characteristic neuronal injury in the hippocampus, and spontaneous recurrent seizures (20). This study investigates CaMKII activity relative to long-standing neuronal injury in the hippocampus in KA-induced experimental temporal lobe epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Calcium/Calmodulin Kinase II Activity of Hippocampus in Kainate-Induced Epilepsy

et al. 2001

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This study investigated calcium/calmodulin kinase II (CaMKII) activity related to long-standing neuronal injury of the hippocampus in kainate (KA)-induced experimental temporal lobe epilepsy. Epileptic seizure was induced by injection of KA (1 g/ L) dissolved in phosphate buffer (0.1 M, pH 7.4) into the left amygdala. Clinical seizures, histopathologic changes and CaMKII activity of the hippocampus were evaluated. Characteristic early limbic and late seizures were developed. Hippocampal CaMKII activity increased significantly 4 and 8 weeks after intra-amygdaloid injection of KA, when late seizures developed. The histopathologic changes of the hippocampus included swelling of neuronal cytoplasm with nuclear pyknosis and loss of neurons in CA3 during this period. The increased activity of CaMKII may correlate with appearance of distant damage in the hippocampus. The above results indicate that intra-amygdaloid injection of KA produces excitatory signals for ipsilateral CA3 neurons in the hippocampus and that subsequently increased levels of CaMKII in postsynaptic neurons induce neuronal injury via phosphorylation of N-methyl-D-aspartate type glutamate receptor.

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“…In the present experiments, we investigated regional accumulation of ZNS in the rat brain by an autoradiographic method, and assessed the effects of ZNS on KA-induced limbic seizures [7][8][9][10][11][12][13][14] by EEG monitoring. In the present study, as soon as the seizure attenuation was recognized by 14 C-ZNS administration, 14 C-ZNS accumulation in the brain was studied.…”

Section: Discussionmentioning

confidence: 99%

Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

Akaike

Tanaka²,

Tojo³

et al. 2001

Can. j. neurol. sci.

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Background:Zonisamide (ZNS) is an antiepileptic drug developed in Japan. Various experimental studies have investigated the effects of ZNS. However, the mechanism of action of ZNS against limbic seizures and secondary generalization is not well-known. We studied ictal regional accumulation of ZNS in the rat brain during kainic acid (KA)-induced limbic status epilepticus.Methods:Fourteen male Wistar rats underwent a stereotactic operation. For recording the electroencephalogram (EEG), electrodes were placed in the left amygdala (LA), left dorsal hippocampus, and over the left sensorimotor cortex. For microinjection, a stainless steel cannula was also inserted into the LA. Seven days after surgery, rats were anesthetized and a catheter was inserted into the femoral vein. The animals were immobilized and allowed to recover from anesthesia for at least two hours. In eight rats, 1.0μL (1.0μg) of KA was injected into the LA, and 1.0 μL of phosphate buffer solution was injected into the LA in six control rats. Sixty minutes after injection, 14C-ZNS was administered intravenously, and an autoradiographic study was done.Results:During limbic status epilepticus, only seizures in the sensorimotor cortex were markedly attenuated a few minutes after 14C-ZNS administration. Additionally, high uptake of 14C-ZNS was noted ipsilaterally in the sensorimotor cortex, parietal cortex and thalamus (lateral portion). In control rats, no EEG change was seen, and distribution of 14C-ZNS was rather homogeneous.Conclusion:These results suggested that ZNS suppresses secondary generalization of limbic seizures by a direct effect on the cerebral cortex.

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Long-term observation of rats after unilateral intra-amygdaloid injection of kainic acid

Cited by 59 publications

References 12 publications

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Calcium/Calmodulin Kinase II Activity of Hippocampus in Kainate-Induced Epilepsy

Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

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Long-term observation of rats after unilateral intra-amygdaloid injection of kainic acid

Cited by 59 publications

References 12 publications

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Experimental Petit Mal-Like Seizure Induced by Microinjection of Kainic Acid Into the Unilateral Mediodorsal Nucleus of the Thalamus

Calcium/Calmodulin Kinase II Activity of Hippocampus in Kainate-Induced Epilepsy

Regional Accumulation of 14C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

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Regional Accumulation of ¹⁴C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures