scholarly journals Deep Prepiriform Cortex Modulates Neuronal Cell Death in Global Ischemia

1997 ◽  
Vol 17 (3) ◽  
pp. 356-360 ◽  
Author(s):  
Kenji Kawaguchi ◽  
Roger P. Simon
Keyword(s):  
Cell Death ◽  
Excitatory Amino Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia ◽  
Glutamate Receptor Antagonist ◽  
Limbic Seizures ◽  
Nmda Glutamate Receptor ◽  
Nmda Glutamate Receptor Antagonist ◽  
Ischemic Neuronal Injury

Deep prepiriform cortex has an important role in modulating neurotransmission during limbic seizures. We used pharmacologic blockade of non- N-methyl-D-aspartate (NMDA) receptors to study excitatory circuitry from the deep prepiriform cortex to the hippocampus during global ischemia in rat. NBQX, a potent non-NMDA glutamate receptor antagonist, was microinjected stereotactically into the deep prepiriform cortex before global ischemia for 10 min. Neuronal cell death in the hippocampus was evaluated quantitatively 72 h after ischemia. The NBQX-injected rats had a greater number of surviving cells in CA1 sector of hippocampus than did saline-injected controls or rats that received NBQX injections 1 mm from the target. Thus, excitatory amino acid-mediated circuitry emanating from deep prepiriform cortex modulates ischemic neuronal injury in the hippocampus.

scholarly journals Ghrelin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

2010 ◽  
Vol 205 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Jiyeon Lee ◽  
Eunjin Lim ◽  
Yumi Kim ◽  
Endan Li ◽  
Seungjoon Park
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Therapeutic Potential ◽  
Excitatory Amino Acid ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Proinflammatory Mediators ◽  
Hippocampal Neurodegeneration

Ghrelin is an endogenous ligand for GH secretagogue receptor type 1a (GHSR1a), and is produced and released mainly from the stomach. It has been recently demonstrated that ghrelin can function as a neuroprotective factor by inhibiting apoptotic pathways. Kainic acid (KA), an excitatory amino acid l-glutamate analog, causes neuronal death in the hippocampus; previous studies suggest that activated microglia and astrocytes actively participate in the pathogenesis of KA-induced hippocampal neurodegeneration. However, it is unclear whether ghrelin has neuroprotective effect in KA-induced hippocampal neurodegeneration. I.p. injection of KA produced typical neuronal cell death in the CA1 and CA3 pyramidal layers of the hippocampus, and the systemic administration of ghrelin significantly attenuated KA-induced neuronal cell death in these regions through the activation of GHSR1a. Ghrelin prevents KA-induced activation of microglia and astrocytes, and the expression of proinflammatory mediators tumor necrosis factor α, interleukin-1β, and cyclooxygenase-2. The inhibitory effect of ghrelin on the activation of microglia and astrocytes appears to be associated with the inhibition of matrix metalloproteinase-3 expression in damaged hippocampal neurons. Our data suggest that ghrelin has a therapeutic potential for suppressing KA-induced pathogenesis in the brain.

scholarly journals Caspase-3-Like Protease Activity-Independent Apoptosis at the Onset of Neuronal Cell Death in the Gerbil Hippocampus after Global Ischemia

2007 ◽  
Vol 30 (10) ◽  
pp. 1950-1953 ◽  
Author(s):  
Hiroki Shimizu ◽  
Makoto Ohgoh ◽  
Masuhiro Ikeda ◽  
Yukio Nishizawa ◽  
Hiroo Ogura
Keyword(s):  
Cell Death ◽  
Protease Activity ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia

A highly sulfated chondroitin sulfate preparation, CS-E, prevents excitatory amino acid-induced neuronal cell death

2007 ◽  
Vol 104 (6) ◽  
pp. 1565-1576 ◽  
Author(s):  
Yoshiaki Sato ◽  
Keiko Nakanishi ◽  
Yoshihito Tokita ◽  
Hiroko Kakizawa ◽  
Michiru Ida ◽  
...  
Keyword(s):  
Cell Death ◽  
Amino Acid ◽  
Chondroitin Sulfate ◽  
Excitatory Amino Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Evaluation of neuronal cell death after a new global ischemia model in infant mice

2003 ◽  
pp. 97-100 ◽  
Author(s):  
Hirokazu Ohtaki ◽  
S. Mori ◽  
T. Nakamachi ◽  
K. Dohi ◽  
L. Yin ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia

scholarly journals Mild Hypothermia Reduces Zinc Translocation, Neuronal Cell Death, and Mortality after Transient Global Ischemia in Mice

2002 ◽  
Vol 22 (10) ◽  
pp. 1231-1238 ◽  
Author(s):  
Daisuke Tsuchiya ◽  
Shwuhuey Hong ◽  
Sang Won Suh ◽  
Takamasa Kayama ◽  
S. Scott Panter ◽  
...  
Keyword(s):  
Cell Death ◽  
Hippocampal Neurons ◽  
Mild Hypothermia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia ◽  
Doppler Flowmetry ◽  
Transient Global Ischemia ◽  
Hematoxylin Eosin ◽  
Cortical Perfusion

The authors sought to determine whether Zn2+ translocation associated with neuronal cell death occurs after transient global ischemia (TGI) in mice, as has been previously shown in rats, and to determine the effect of mild hypothermia on this reaction. To validate the TGI model, carbon-black injection and laser-Doppler flowmetry were compared in three strains of mice (C57BL/6, SV129, and HSP70 transgenic mice) to assess posterior communicating artery (PcomA) development and cortical perfusion. In C57BL/6 mice, optimal results were obtained when subjected to 20-minute TGI. Brain and rectal temperature measurements were compared to monitor hypothermia. Results of TGI were compared in normothermia (NT; 37°C) and mild hypothermia groups (HT; 33°C) by staining with Zn2+-specific fluorescent dye, N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) and hematoxylin– eosin 72 hours after reperfusion. The Zn2+ translocation observed in hippocampus CA1, CA2, and Hilus 72 hours after 20 minutes of TGI was significantly reduced by mild hypothermia. The number of degenerating neurons in the HT group was significantly less than in the NT group. Mild hypothermia reduced mortality significantly (7.1% in HT, 42.9% in NT). Results suggest that mild hypothermia may reduce presynaptic Zn2+ release in mice, which protects vulnerable hippocampal neurons from ischemic necrosis. Future studies may further elucidate mechanisms of Zn2+-induced ischemic injury.

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