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Origin of ischemia-induced glutamate release in the gerbil hippocampus
S186 1 l-04
STRIATAL CELL GRAFTS IN THE ISCHEMTC STRIATUM OF RATS IXCREASE GABA OF PASSJVII RELEASE, GABAa RECEPTOR EXPRESSTON AND IMPROVE TIIE PERFORMANCE AVOIDANCE AND WATER MAZE TASKS. HIT00 NISHISO, TAKES111 HASIIITANJ. TERUMl S.AKI!R,\I . YOSHIAKI ISOBE, KAZUO KOIDEI, NORITAKA AIH
Striatal cells were grafted in the ischcmic striatum of rats af'ter intraluminal occlusion of the middle ccrcbrnl artery (MCA). The survival of grafted cells, GABA release, GABA* receptor expression nnd behavioral recovery wet-e investigated. One hour occlusion of the MCA induced ischemic infarcts mainly in the lateral part of the striatum. Although the size of the infarcts asscsscd by MRI was variable, each animal exhibited deficits in passive avoidance and water maze tasks. In ischemic animals, pallidal GABA decreased to about half of the control level. Fetal striatal cell suspensions were grafted in the infarcted striata 2 to 4 weeks after the induction of ischcmia. After the graft, pcrformancc in passive avoidance/water mnzc tasks was improved, GABA levels recovered and GABA, receptors were reorganized. Data indicntc that striatal cell grafts in the ischemic striatum reconstruct the strintopnllidnl pathway and ameliorate bchnvioral deficits.
1 l-05
REGIONAL DIFFERENCES IN FATTY ACID RELEASE FROM HIPPOCAMPUS UNDER HYPOXIA AND HYPOGLYCEMIA. SUSUMU ANDO, KAZUO KON,
HATSUE WAKI AND YASUKAZU TANAKA, Department of Membrane Biochemistry, Gerontology, 35-2 Sakaecho, Itabashi-ku. Tokyo 173, Japan
Tokyo Metropolitan Institute of
An increase of free fatty acids in brain tissue following ischemic insult may indicate the initiation of membrane damages. Brain ischemia can be simulated by subjecting brain slices to hypoxic and hypoglycemic conditions in vitro. This system may provide a model for understanding the mechanisms of neuronal membrane damage and functional deterioration. Hippocampal slices maintained in an oxygenated glucose containing medium were placed under various conditions: hypoxia, hypoglycemia, and hypoxia + hypoglycemia. The slices were dissected into two parts, CA1 rich and CA3 rich regions. They were analyzed by an enzyme method for detecting that CA1 region is intrisically more free fatty acid release. Release was higher in CAl. This suggests vulnerable than CA3 region when suffering from the same severity of ischemia. In a parallel synaptosomes were shown to release fatty acids when subjected to hypoxia plus experiment, This may imply that ischemia-induced membrane hypoglycemia, and to decrease acetylcholine release. damages impair the neurotransmission processes.
1 l-06
ORIGIN OF ISCHEMIA-INDUCED GLUTAMATE RELEASE IN THE GERBIL HIPPOCAMPUS. YASUSHI ANDOU, AKIRA MITANI AND KIYOSHI KATAOKA, Department of Physiology, School of Medicine, Ehime University, Shigenobu, Onsen-gun, Ehime 791-02, Japan
We previously demonstrated that glutamate was excessively released in field CA1 of the gerbil hippocampus during 5-min ischemia. In the present study, the origin of the glutamate was investigated by microdialysis. A probe (OSmm-long-membrane) was positioned in the white matter of the cerebral cortex in normal animals or in field CA1 of the hippocampus in animals which had been subjected to 5-min ischemia lo-14 days prior to the cxperimcnt to produce degeneration of the CA1 pyramidal neurons and presynaptic terminals. No significant changes in glutamate release were observed. When a probe was positioned in field CA1 in which presynaptic terminals from ipsi- and contralateral CA3 pyramidal neurons had been eliminated by kainate injection into the lateral ventricles 4-7 days before the experiment, a significant increase in glutamate release was observed as well as a delay in the increase of release of glutamate. These data suggest that glial cells are not the source of the glutamate whose release is induced during transient 5-min ischemia, that glutamate is released presynaptically during the early stage of 5-min ischemia and is mainly released from postsynaptic components(CA1 pyramidal neurons) during the late stage of 5-min ischemia.
STRIATAL CELL GRAFTS IN THE ISCHEMTC STRIATUM OF RATS IXCREASE GABA OF PASSJVII RELEASE, GABAa RECEPTOR EXPRESSTON AND IMPROVE TIIE PERFORMANCE AVOIDANCE AND WATER MAZE TASKS. HIT00 NISHISO, TAKES111 HASIIITANJ. TERUMl S.AKI!R,\I . YOSHIAKI ISOBE, KAZUO KOIDEI, NORITAKA AIH
Striatal cells were grafted in the ischcmic striatum of rats af'ter intraluminal occlusion of the middle ccrcbrnl artery (MCA). The survival of grafted cells, GABA release, GABA* receptor expression nnd behavioral recovery wet-e investigated. One hour occlusion of the MCA induced ischemic infarcts mainly in the lateral part of the striatum. Although the size of the infarcts asscsscd by MRI was variable, each animal exhibited deficits in passive avoidance and water maze tasks. In ischemic animals, pallidal GABA decreased to about half of the control level. Fetal striatal cell suspensions were grafted in the infarcted striata 2 to 4 weeks after the induction of ischcmia. After the graft, pcrformancc in passive avoidance/water mnzc tasks was improved, GABA levels recovered and GABA, receptors were reorganized. Data indicntc that striatal cell grafts in the ischemic striatum reconstruct the strintopnllidnl pathway and ameliorate bchnvioral deficits.
1 l-05
REGIONAL DIFFERENCES IN FATTY ACID RELEASE FROM HIPPOCAMPUS UNDER HYPOXIA AND HYPOGLYCEMIA. SUSUMU ANDO, KAZUO KON,
HATSUE WAKI AND YASUKAZU TANAKA, Department of Membrane Biochemistry, Gerontology, 35-2 Sakaecho, Itabashi-ku. Tokyo 173, Japan
Tokyo Metropolitan Institute of
An increase of free fatty acids in brain tissue following ischemic insult may indicate the initiation of membrane damages. Brain ischemia can be simulated by subjecting brain slices to hypoxic and hypoglycemic conditions in vitro. This system may provide a model for understanding the mechanisms of neuronal membrane damage and functional deterioration. Hippocampal slices maintained in an oxygenated glucose containing medium were placed under various conditions: hypoxia, hypoglycemia, and hypoxia + hypoglycemia. The slices were dissected into two parts, CA1 rich and CA3 rich regions. They were analyzed by an enzyme method for detecting that CA1 region is intrisically more free fatty acid release. Release was higher in CAl. This suggests vulnerable than CA3 region when suffering from the same severity of ischemia. In a parallel synaptosomes were shown to release fatty acids when subjected to hypoxia plus experiment, This may imply that ischemia-induced membrane hypoglycemia, and to decrease acetylcholine release. damages impair the neurotransmission processes.
1 l-06
ORIGIN OF ISCHEMIA-INDUCED GLUTAMATE RELEASE IN THE GERBIL HIPPOCAMPUS. YASUSHI ANDOU, AKIRA MITANI AND KIYOSHI KATAOKA, Department of Physiology, School of Medicine, Ehime University, Shigenobu, Onsen-gun, Ehime 791-02, Japan
We previously demonstrated that glutamate was excessively released in field CA1 of the gerbil hippocampus during 5-min ischemia. In the present study, the origin of the glutamate was investigated by microdialysis. A probe (OSmm-long-membrane) was positioned in the white matter of the cerebral cortex in normal animals or in field CA1 of the hippocampus in animals which had been subjected to 5-min ischemia lo-14 days prior to the cxperimcnt to produce degeneration of the CA1 pyramidal neurons and presynaptic terminals. No significant changes in glutamate release were observed. When a probe was positioned in field CA1 in which presynaptic terminals from ipsi- and contralateral CA3 pyramidal neurons had been eliminated by kainate injection into the lateral ventricles 4-7 days before the experiment, a significant increase in glutamate release was observed as well as a delay in the increase of release of glutamate. These data suggest that glial cells are not the source of the glutamate whose release is induced during transient 5-min ischemia, that glutamate is released presynaptically during the early stage of 5-min ischemia and is mainly released from postsynaptic components(CA1 pyramidal neurons) during the late stage of 5-min ischemia.