Kainic acid induces long-lasting depolarizations in hippocampal neurons only when applied to stratum lucidum

1988 ◽  
Vol 72 (1) ◽  
pp. 135-140 ◽  
Author(s):  
S. Sawada ◽  
M. Higashima ◽  
C. Yamamoto
Keyword(s):  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Stratum Lucidum

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.

Melatonin protects hippocampal neurons in vivo against kainic acid-induced damage in mice

1998 ◽  
Vol 54 (3) ◽  
pp. 382-389 ◽  
Author(s):  
Dun-xian Tan ◽  
Lucien C. Manchester ◽  
Russel J. Reiter ◽  
Wenbo Qi ◽  
Seok Joong Kim ◽  
...  
Keyword(s):  
Kainic Acid ◽  
Hippocampal Neurons

Fatty acid amide hydrolase inhibitor URB597 may protect against kainic acid–induced damage to hippocampal neurons: Dependence on the degree of injury

2017 ◽  
Vol 137 ◽  
pp. 84-94 ◽  
Author(s):  
Irina B. Mikheeva ◽  
Liubov Shubina ◽  
Nataliya Matveeva ◽  
Luybov L. Pavlik ◽  
Valentina F. Kitchigina
Keyword(s):  
Fatty Acid ◽  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

scholarly journals Effects of scorpion venom heat-resistant peptide on the hippocampal neurons of kainic acid-induced epileptic rats

2021 ◽  
Vol 54 (5) ◽  
Author(s):  
Qizuan Chen ◽  
Pengfan Yang ◽  
Qiao Lin ◽  
Jiasheng Pei ◽  
Yanzeng Jia ◽  
...  
Keyword(s):  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Scorpion Venom ◽  
Heat Resistant

MicroRNA-451 Aggravates Kainic Acid-induced Seizure and Neuronal Apoptosis by Targeting GDNF

2020 ◽  
Vol 17 (1) ◽  
pp. 50-57 ◽  
Author(s):  
Ning Weng ◽  
Jingbo Sun ◽  
Shixiang Kuang ◽  
Hai Lan ◽  
Qiansong He ◽  
...  
Keyword(s):  
Kainic Acid ◽  
Hippocampal Neurons ◽  
Neuronal Apoptosis ◽  
Neuronal Damage ◽  
Morphological Changes ◽  
Potential Contribution ◽  
Mice Model ◽  
Nissl Staining ◽  
Seizure Models

Aim: Epilepsy is a common and serious neurological disease that causes recurrent episodes, but its molecular mechanism remains unclear. Abnormal miRNA expression is associated with epilepsy, including miR-451. This research investigated the role of miR-451 in seizure and its detailed mechanism. Methods: The seizure mice model was induced by kainic acid (KA) injection to the right lateral cerebral ventricle. Behavioral changes in mice were observed and evaluated by the Racine Scale. The miR-451 knockout mice were established by adenovirus infection. The in vitro model was performed by miR-451 mimics transfected HEK-293 cells. The amount of neuronal death and morphological changes were evaluated by Nissl staining and H&E staining. Results: The results showed that miR-451 is up regulated in KA-induced seizure models and miR- 451 knockout decreased the behavior score and improved the pathological changes of the hippocampus. Besides, MiR-451 knockout inhibited the apoptosis of hippocampal neurons. Bioinformatics studies have shown that glial cell line-derived neurotrophic factor (GDNF) is a target gene of miR-451. MiR-451 could negatively regulate the expression of GDNF. GDNF overexpression could reverse the effect of miR-451 on KA induced brain injury and neuronal apoptosis. Conclusion: This research demonstrates that miR-451 can affect the behavior of KA-induced epilepsy mice and hippocampal neuronal damage by regulating GDNF expression. The results would provide an experimental foundation for further research about the potential contribution of mi- RNAs to epilepsy pathophysiology.

Overexpression of PDZ1 domain prevents apoptosis of rat hippocampal neurons induced by kainic acid

2009 ◽  
Vol 460 (2) ◽  
pp. 133-137 ◽  
Author(s):  
Shu-Qun Hu ◽  
Yan-Yan Zong ◽  
Le-Ming Fan ◽  
Guang-Yi Zhang
Keyword(s):  
Kainic Acid ◽  
Hippocampal Neurons
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