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Kainic acid-induced neurodegenerative model: potentials and limitations.

Zheng XY, Zhang HL, Luo Q, Zhu J - J. Biomed. Biotechnol. (2010)

Bottom Line: Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD).Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS.This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, The First Hospital of Jilin University, Changchun, China.

ABSTRACT
Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such as α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

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The molecular structure of kainic acid (2-carboxy-4-isopropenylpyrrolidin-3-ylacetic acid, KA). The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 g/mol.
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fig1: The molecular structure of kainic acid (2-carboxy-4-isopropenylpyrrolidin-3-ylacetic acid, KA). The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 g/mol.

Mentions: KA was originally isolated from the seaweed called “Kainin-sou” or “Makuri”. The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 (Figure 1). Initially, KA was used as an antihelminth compound to remove worms from the gut. Subsequent studies indicated that KA is a nondegradable analog of glutamate and a potent neurotoxin [1]. KA exerts its neuroexcitotoxic and epileptogenic properties by acting on kainate receptors (KARs). Upon binding to KARs, KA induces a number of cellular events, including the influx of cellular Ca2+, production of reactive oxygen species (ROS), and mitochondrial dysfunction leading to neuronal apoptosis and necrosis [2]. KA has been extensively utilized as a specific agonist for ionotropic glutamate receptors (iGluRs); that is, KARs to mimic the effect of glutamate in neurodegenerative models, as well as to distinguish other ionotropic receptors for glutamate. KARs mediate most of kainate-induced seizures and excitotoxic neuronal death, whereby serving as a promising therapeutic target for neurodegeneration.


Kainic acid-induced neurodegenerative model: potentials and limitations.

Zheng XY, Zhang HL, Luo Q, Zhu J - J. Biomed. Biotechnol. (2010)

The molecular structure of kainic acid (2-carboxy-4-isopropenylpyrrolidin-3-ylacetic acid, KA). The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 g/mol.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2992819&req=5

fig1: The molecular structure of kainic acid (2-carboxy-4-isopropenylpyrrolidin-3-ylacetic acid, KA). The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 g/mol.
Mentions: KA was originally isolated from the seaweed called “Kainin-sou” or “Makuri”. The molecular formula of KA are C10H15NO4 and the molar mass of KA is 213.23 (Figure 1). Initially, KA was used as an antihelminth compound to remove worms from the gut. Subsequent studies indicated that KA is a nondegradable analog of glutamate and a potent neurotoxin [1]. KA exerts its neuroexcitotoxic and epileptogenic properties by acting on kainate receptors (KARs). Upon binding to KARs, KA induces a number of cellular events, including the influx of cellular Ca2+, production of reactive oxygen species (ROS), and mitochondrial dysfunction leading to neuronal apoptosis and necrosis [2]. KA has been extensively utilized as a specific agonist for ionotropic glutamate receptors (iGluRs); that is, KARs to mimic the effect of glutamate in neurodegenerative models, as well as to distinguish other ionotropic receptors for glutamate. KARs mediate most of kainate-induced seizures and excitotoxic neuronal death, whereby serving as a promising therapeutic target for neurodegeneration.

Bottom Line: Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD).Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS.This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, The First Hospital of Jilin University, Changchun, China.

ABSTRACT
Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such as α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

Show MeSH
Related in: MedlinePlus