scholarly journals CD200 Change Is Involved in Neuronal Death in Gerbil Hippocampal CA1 Field Following Transient Forebrain Ischemia and Postischemic Treatment with Risperidone Displays Neuroprotection without CD200 Change

2021 ◽  
Vol 22 (3) ◽  
pp. 1116
Author(s):  
Tae-Kyeong Lee ◽  
Myoung Cheol Shin ◽  
Ji Hyeon Ahn ◽  
Dae Won Kim ◽  
Bora Kim ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Microglial Activation ◽  
Pyramidal Neurons ◽  
Neuronal Loss ◽  
Gabaergic Neurons ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Hippocampal Ca1 ◽  
Hippocampus Proper ◽  
Hippocampal Ca1 Field

It has been reported that CD200 (Cluster of Differentiation 200), expressed in neurons, regulates microglial activation in the central nervous system, and a decrease in CD200 expression causes an increase in microglial activation and neuronal loss. The aim of this study was to investigate time-dependent changes in CD200 expression in the hippocampus proper (CA1, 2, and 3 fields) after transient forebrain ischemia for 5 min in gerbils. In this study, 5-min ischemia evoked neuronal death (loss) of pyramidal neurons in the CA1 field, but not in the CA2/3 fields, at 5 days postischemia. In the sham group, CD200 expression was found in pyramidal neurons of the CA1 field, and the immunoreactivity in the group with ischemia was decreased at 6 h postischemia, dramatically increased at 12 h postischemia, decreased (to level found at 6 h postischemia) at 1 and 2 days postischemia, and significantly increased again at 5 days postischemia. At 5 days postischemia, CD200 immunoreactivity was strongly expressed in microglia and GABAergic neurons. However, in the CA3 field, the change in CD200 immunoreactivity in pyramidal neurons was markedly weaker than that in the CA1 field, showing there was no expression of CD 200 in microglia and GABAergic neurons. In addition, treatment of 10 mg/kg risperidone (an atypical antipsychotic drug) after the ischemia hardly changed CD200 immunoreactivity in the CA1 field, showing that CA1 pyramidal neurons were protected from the ischemic injury. These results indicate that the transient ischemia-induced change in CD200 expression may be associated with specific and selective neuronal death in the hippocampal CA1 field following transient forebrain ischemia.

scholarly journals Calcium Movement in Ischemia-Tolerant Hippocampal CA1 Neurons after Transient Forebrain Ischemia in Gerbils

1996 ◽  
Vol 16 (5) ◽  
pp. 915-922 ◽  
Author(s):  
Shinsuke Ohta ◽  
Shigeru Furuta ◽  
Ichiro Matsubara ◽  
Keiji Kohno ◽  
Yoshiaki Kumon ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Neuronal Death ◽  
Pyramidal Neurons ◽  
Forebrain Ischemia ◽  
Electron Microscopic ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Before And After ◽  
Intracellular Ca

Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracelluar Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca2+-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca2+-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca2+-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequestration and plasma membrane Ca2+-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.

Increase of galectin-3 expression in microglia by hyperthermia in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia

2011 ◽  
Vol 504 (3) ◽  
pp. 199-203 ◽  
Author(s):  
Kunio Satoh ◽  
Masayuki Niwa ◽  
Nguyen Huy Binh ◽  
Masaya Nakashima ◽  
Kazuhiro Kobayashi ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Delayed Neuronal Death ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Hippocampal Ca1 ◽  
Galectin 3

scholarly journals Selective Proteasomal Dysfunction in the Hippocampal CA1 Region after Transient Forebrain Ischemia

2002 ◽  
Vol 22 (6) ◽  
pp. 705-710 ◽  
Author(s):  
Akio Asai ◽  
Nobuyuki Tanahashi ◽  
Jian-hua Qiu ◽  
Nobuhito Saito ◽  
Shunji Chi ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Neuronal Death ◽  
Proteasome Activity ◽  
26S Proteasome ◽  
Delayed Neuronal Death ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

Delayed neuronal death in the hippocampal CA1 region after transient forebrain ischemia may share its underlying mechanism with neurodegeneration and other modes of neuronal death. The precise mechanism, however, remains unknown. In the postischemic hippocampus, conjugated ubiquitin accumulates and free ubiquitin is depleted, suggesting impaired proteasome function. The authors measured regional proteasome activity after transient forebrain ischemia in male Mongolian gerbils. At 30 minutes after ischemia, proteasome activity was 40% of normal in the frontal cortex and hippocampus. After 2 hours of reperfusion, it had returned to normal levels in the frontal cortex, CA3 region, and dentate gyrus, but remained low for up to 48 hours in the CA1 region. Thus, the 26S proteasome was globally impaired in the forebrain during transient ischemia and failed to recover only in the CA1 region after reperfusion. The authors also measured 20S and 26S proteasome activities directly after decapitation ischemia (at 5 and 20 minutes) by fractionating the extracts with glycerol gradient centrifugation. Without adenosine triphosphate (ATP), only 20S proteasome activity was detected in extracts from both the hippocampus and frontal cortex. When the extracts were incubated with ATP in an ATP-regenerating system, 26S proteasome activity recovered almost fully in the frontal cortex but only partially in the hippocampus. Thus, after transient forebrain ischemia, ATP-dependent reassociation of the 20S catalytic and PA700 regulatory subunits to form the active 26S proteasome is severely and specifically impaired in the hippocampus. The irreversible loss of proteasome function underlies the delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 region.

Galectin-3 expression in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia, and its inhibition by hypothermia

2011 ◽  
Vol 1382 ◽  
pp. 266-274 ◽  
Author(s):  
Kunio Satoh ◽  
Masayuki Niwa ◽  
Wael Goda ◽  
Nguyen Huy Binh ◽  
Masaya Nakashima ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Delayed Neuronal Death ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Hippocampal Ca1 ◽  
Galectin 3
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