Excitatory Amino Acid Binding Sites in the Rat Hippocampus after Transient Forebrain Ischemia

The influence of transient forebrain ischemia on the temporal alteration of glutamate receptors in the hippocampal formation was analyzed by means of in vitro quantitative receptor autoradiography. We compared the binding of N-methyl-d-aspartate (NMDA) receptors using [3H]3-((±)2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), noncompetitive NMDA antagonist binding sites using [3H]N-(1-(2-thienyl)-cyclohexyl)-3,4-piperidine (TCP), and kainate (KA) receptors. In the CA1 subfield of the hippocampus, the number of NMDA receptors and noncompetitive NMDA antagonist binding sites remained constant during the early stage of recirculation when the CA1 pyramidal cells remained histologically intact. A significant reduction of these receptor densities was observed 7 days following ischemia, when NMDA receptors and noncompetitive NMDA antagonist binding sites lost 64 and 29% of their binding sites in the stratum radiatum of the CA1, respectively. The KA receptor density in the CA1 subfield decreased by 44% 7 days after ischemia. Marked loss of the above-mentioned receptors in the CA1 after selective depletion of the CA1 pyramidal cells indicated that NMDA receptors, noncompetitive NMDA antagonist binding sites, and KA receptors in the CA1 are predominantly localized on the CA1 pyramidal cells. NMDA receptor density in the CA3 gradually decreased during the recirculation period. The stratum moleculare of the dentate gyrus, whose structure was histologically intact after ischemic insult, also showed a reduction of NMDA receptors 7 days following ischemia. [3H]KA receptor density in the stratum lucidum of the CA3 and in the hilus also decreased during recirculation. These results indicate that postischemic change of neuronal activity was not restricted to the ischemic-lesioned CA1 but that the histologically intact CA3 and dentate gyrus had also modulated neuronal transmission after ischemia.

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Fractalkine-immunoreactivity increases in the hippocampal CA1 pyramidal cells after transient forebrain ischemia

Neuroscience Research ◽

10.1016/s0168-0102(00)81710-1 ◽

2000 ◽

Vol 38 ◽

pp. S144

Author(s):

A Nishiyori

Keyword(s):

Pyramidal Cells ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Ca1 Pyramidal Cells ◽

Hippocampal Ca1

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Depressed Responses to Applied and Synaptically-Released GABA in CA1 Pyramidal Cells, but not in CA1 Interneurons, after Transient Forebrain Ischemia

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/sj.jcbfm.9600171 ◽

2005 ◽

Vol 26 (1) ◽

pp. 112-124 ◽

Cited By ~ 13

Author(s):

Ren-Zhi Zhan ◽

J Victor Nadler ◽

Rochelle D Schwartz-Bloom

Keyword(s):

Pyramidal Cells ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Ca1 Pyramidal Cells

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Caspase activation as an apoptotic evidence in the gerbil hippocampal CA1 pyramidal cells following transient forebrain ischemia

Neuroscience Letters ◽

10.1016/s0304-3940(01)01559-2 ◽

2001 ◽

Vol 300 (2) ◽

pp. 103-106 ◽

Cited By ~ 35

Author(s):

Masayuki Niwa ◽

Akira Hara ◽

Tomohiko Iwai ◽

Shaotan Wang ◽

Koichi Hotta ◽

...

Keyword(s):

Pyramidal Cells ◽

Forebrain Ischemia ◽

Caspase Activation ◽

Transient Forebrain Ischemia ◽

Ca1 Pyramidal Cells ◽

Hippocampal Ca1

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Molecular cloning of rat cDNA for cytosolic phospholipase A2 and the increased gene expression in the dentate gyrus following transient forebrain ischemia [Molecular Brain Research 25 (1994) 364–368]

Molecular Brain Research ◽

10.1016/0169-328x(94)90023-x ◽

1994 ◽

Vol 27 (2) ◽

pp. 355 ◽

Cited By ~ 2

Author(s):

Y. Owada ◽

T. Tominaga ◽

T. Yoshimoto ◽

H. Kondo

Keyword(s):

Gene Expression ◽

Phospholipase A2 ◽

Dentate Gyrus ◽

Molecular Cloning ◽

Brain Research ◽

Cytosolic Phospholipase A2 ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Cytosolic Phospholipase ◽

Molecular Brain

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Differential responses between CA1 pyramidal cells and dentate gyrus granule cells to ischemia-like conditions in rat hippocampal slices

Neuroscience Research Supplements ◽

10.1016/0921-8696(94)92336-1 ◽

1994 ◽

Vol 19 ◽

pp. S27

Author(s):

Hitoshi Shimizu ◽

Akira Mizuguchi ◽

Mamoru Aoki

Keyword(s):

Dentate Gyrus ◽

Granule Cells ◽

Hippocampal Slices ◽

Pyramidal Cells ◽

Ca1 Pyramidal Cells ◽

Differential Responses

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Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

Nutrients ◽

10.3390/nu12082477 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2477

Author(s):

Bora Kim ◽

Tae-Kyeong Lee ◽

Cheol Woo Park ◽

Dae Won Kim ◽

Ji Hyeon Ahn ◽

...

Keyword(s):

Pyramidal Neurons ◽

Neuroprotective Effect ◽

Ischemic Injury ◽

Pyramidal Cells ◽

Acid Oxidation ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Ca1 Region ◽

Pine Tree ◽

Before And After

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

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Regional Differences in Late-Onset Iron Deposition, Ferritin, Transferrin, Astrocyte Proliferation, and Microglial Activation after Transient Forebrain Ischemia in Rat Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1995.27 ◽

1995 ◽

Vol 15 (2) ◽

pp. 216-226 ◽

Cited By ~ 74

Author(s):

Yoichi Kondo ◽

Norio Ogawa ◽

Masato Asanuma ◽

Zensuke Ota ◽

Akitane Mori

Keyword(s):

Rat Brain ◽

Parietal Cortex ◽

Neuronal Death ◽

Late Onset ◽

Neuronal Damage ◽

Pyramidal Cells ◽

Iron Deposition ◽

Forebrain Ischemia ◽

Transient Forebrain Ischemia ◽

Layer V

With use of iron histochemistry and immuno-histochemistry, regional changes in the appearance of iron, ferritin, transferrin, glial fibrillary acidic protein–positive astrocytes, and activated microglia were examined from 1 to 24 weeks after transient forebrain ischemia (four-vessel occlusion model) in rat brain. Expression of the C3bi receptor and the major histocompatibility complex class II antigen was used to identify microglia. Neuronal death was confirmed by hematoxylin–eosin staining only in pyramidal cells of the hippocampal CA, region, which is known as the area most vulnerable to ischemia. Perls' reaction with 3,3′-diaminobenzidine intensification revealed iron deposits in the CA, region after week 4, which gradually increased and formed clusters by week 24. Iron also deposited in layers III-V of the parietal cortex after week 8 and gradually built up as granular deposits in the cytoplasm of pyramidal cells in frontocortical layer V. An increasing astroglial reaction and the appearance of ferritin-immunopositive microglia paralleled the iron accumulation in the hippocampal CA, region, indicating that iron deposition was probably produced in the process of gliosis. Neither neuronal death nor atrophy was found in the cerebral cortex. Nevertheless, an astroglial and ferritin-immunopositive microglial reaction became evident at week 8 in the parietal cortex. On the other hand, the granular iron deposition in the pyramidal neurons of frontocortical layer V was not accompanied by any glial reaction in the chronic stage of ischemia. Three different types of iron deposition in the chronic phase after transient forebrain ischemia were shown in this study. In view of the neuronal damage caused by iron-catalyzed free radical formation, the late-onset iron deposition may be relevant to the pathogenesis of the chronic brain dysfunction seen at a late stage after cerebral ischemia.

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