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Establishment of neurophysiologic classification of the symptomatic epilepsy and molecular pathologic study on the mechanisms of occurrence of epilepsy.

Research Project

Project/Area Number 10839008
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 動物臨床医学
Research InstitutionTottori University

Principal Investigator

KAGOTA Katsumoto  Faculty of Agriculture, Tottori University, Professor, 農学部, 教授 (80091437)

Co-Investigator(Kenkyū-buntansha) TAKEUCHI Takashi  Faculty of Agriculture, Tottori University, Research Assistant, 農学部, 助手 (20216849)
MORITA Takehito  Faculty of Agriculture, Tottori University, Research Assistant, 農学部, 助手 (70273901)
SHIMADA Akinori  Faculty of Agriculture, Tottori University, Professor, 農学部, 教授 (20216055)
SATOH Kota  Faculty of Agriculture, Tottori University, Research Assistant, 農学部, 助手 (50283974)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥2,600,000 (Direct Cost: ¥2,600,000)
Keywordselectroencephalography / epilepsy / symptomatic / dog
Research Abstract

A male Maltese dog gradually showed various clinical signs such as inappropriate vocalization, aggression, agitation, circling and generalized seizure at 1-year-old age. A blood biochemistry showed an elevated value of ammonia (51 N-μ g/dl). Electroencephalography (EEG) analysis revealed that epileptic foci were detected in the frontal, parietal, temporal and occipital lobes. A significant glutamate value was found in the cerebrospinal fluid. Computed tomography examination disclosed multiple low density area in the cerebral cortex and white matter. Angiographic analysis disclosed portal-shunt. Histologically, naked astroglial cells were noted throughout the cerebral cortices. Immunohistologically, low expression of glutamine synthetase (GS) comparing to those in the control dogs. GS is a ubiquitous enzyme that catalyzes the ATP-dependent conversion of glutamate (excitatory neurotransmitter) to glutamine using ammonia as the nitrogen source. An abnormal metabolism of glutamate in the brain may be related with superexcitation of neurons.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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