2001 Fiscal Year Final Research Report Summary
AMYGDALOID KINDLING IN GLUTAMATE TRANSPORTER (GLAST < GLT-1) KNOCKOUT MICE
| Project/Area Number |
12670946
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | MIYAZAKI MEDICAL COLLEGE |
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Principal Investigator |
TSURU Noriko Miyazaki Medical College, School of Medicine, Psychology, Professor, 医学部, 教授 (90041425)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIDA Yasushi Miyazaki Medical College, School of Medicine, Psychiatry, Assistant Professor, 医学部, 助教授 (20212897)
UEDA Yuto Miyazaki Medical College, School of Medicine, Psychiatry, Instructor, 医学部, 講師 (70244192)
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| Project Period (FY) |
2000 – 2001
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| Keywords | KINDLING / GLUTAMATE / TRANSPORTER / GLAST / TRANSGENIC / MOUSE / EPILEPTOGENESIS / EEG |
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| Research Abstract |
Glutamate is a predominant excitatory neurotransmitter in the mammalian central nervous system. We previously reported the abnormal glutamate release during seizures following kindling. GLAST and GLT-1 are astrocytic glutamate transporters, highly concentrated in the cerebellum and the telencephalon, respectively. We have investigated whether stages of amygdala kindling in knockout (KO) mice deficient GLAST are the same as those of wild mice and whether there is secondary epileptogenesis. Method : Electrodes were implanted into the basolateral amygdala (B2.0, L3.0, H-4.5) in C57BL/6J mice and GLAST KO mice under the anesthesia. Once-daily stimulation of biphasic square pulse was applied through the stimulation electrodes. Results : The behavioral changes of the kindling in mice were : 1) arrest of behavior, 2) head nodding, 3) forelimb clonus, 4) dual forelimb clonus with rearing, 5) tonic generalized convulsion with elevation of tail, falling with GTC. There was a significant difference in the development of kindling. More stimulation was required for the kindling in GLAST deficient mice. There was no difference in the duration of AD between control and GLAST KO mice until the 16^<th> stimulations. However, the afterdischarges became slightly longer following overkindling in the control mice. The numbers of spikes at the stimulation point and secondary site in the GLAST KO mice were greater than those of control mice. These results suggest to us the GLAST (cerebellar glutamate transporter) may have a role in secondary epileptogenesis.
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