title: Electrophysiological, behavioral and metabolical features of globus pallidus seizures induced by a microinjection of kainic acid in rats.
abstract: There has been few studies of the globus pallidus in relation to epilepsy. In this study, kainic acid (KA)-induced globus pallidus seizure was electrophysiologically, electroencephalographically, histopathologically and metabolically investigated in rats. Sixteen Wistar rats weighing 250-350 g were used. Under intraperitoneal pentobarbital anesthesia, a stainless-steel cannula was inserted stereotaxically into the left globus pallidus pars externa (GPe) for KA injection. For recording EEG, a depth electrode was inserted into the left GPe, just posterior to the tip of the injection guide cannula. Electrodes were also inserted into the right globus pallidus and bilateral sensorimotor cortex (SMC). EEG changes after KA injection were classified as follows: Continuous low-voltage spikes were observed in the left GPe on EEG at stage 1. Intermittent multiple spikes and wave complexes began to propagate to the left SMC at stage 2. Continuous spikes and wave complexes began to propagate to the bilateral SMC at stage 3. Secondary generalized seizures were observed at stage 4. Globus pallidus seizures recurred every 7-9 min and lasted for 4-6 h. However, the seizures gradually subsided and became normal within 18 h. No spontaneous seizure was detected for the next 30 days. Histopathological study revealed a small gliotic lesion with neuronal cell loss around the cannula tip. Neither degeneration nor neuronal cell loss in the ipsilateral hippocampus were observed. The autoradiogram using [14C]2-deoxyglucose during seizure status demonstrated a remarkable increase of local cerebral glucose utilization not only in the GPe but also in the GPi. An increase glucose metabolism was also found in the follows: the medial and lateral septal nucleus, substantia nigra, hippocampus, frontal cortex, parietal cortex, piriform cortex, entorhinal cortex, accumbens nucleus, ventral and lateral nucleus of the thalamus, amygdala, and ventral nucleus of hypothalamus. KA injection into the unilateral GPe evoked not only epileptic excitation of the cortex but also transient enhancement of the globus pallidus-substantia nigra circuit.
authors.affiliation: Department of Neurosurgery, Asahikawa Medical College, 2-1, Midorigaoka-Higashi, 078-8510 Asahikawa, Japan. samy@mvj.biglobe.ne.jp
authors.forename: Atsushi
authors.initials: A
authors.lastname: Sawamura
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Hashizume
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Tanaka
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D002250:Carbon Radioisotopes; D003847:Deoxyglucose; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D004827:Epilepsy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D005062:European Union; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D007839:Functional Laterality / Q000502:physiology; D005917:Globus Pallidus / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009069:Movement Disorders / Q000378:metabolism / Q000503:physiopathology; D009410:Nerve Degeneration / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002250:Carbon Radioisotopes; D018690:Excitatory Amino Acid Agonists; D003847:Deoxyglucose; D005947:Glucose; D007608:Kainic Acid