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Kainic acid


CAS No. : 487-79-6

487-79-6
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Cat. No. : HY-N2309
M.Wt: 213.23
Formula: C10H15NO4
Purity: >98 %
Solubility: H2O : 10 mg/mL (ultrasonic;warming;heat to 60°C);DMSO : 40 mg/mL (ultrasonic)
Introduction of 487-79-6 :

Kainic acid is a potent excitotoxic agent. Kainic acid hydrate also is an agonist for a subtype of ionotropic glutamate receptor. Kainic acid induces seizures[1][2]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Kainic acid-induced epilepsy model is an effective tool for studying temporal lobe epilepsy (TLE) and can be administered systemically, into the hippocampus, or amygdala, and is reproducible in various animal models. The systemic Kainic acid model closely resembles human TLE. When Kainic acid (5 nM) is injected into the neostriatum, substantia nigra, or cerebellum, over half of the compound disappears from the injection site and brain within 0.5 hours, with radioactivity detected in other brain regions at concentrations below 7 pM/mg tissue[3][4][6].

1. Induction of epilepsy model in mouse[5]
Background
Kainic acid, an analog of L-glutamate and an ionotropic KA receptor agonist, can damage hippocampal pyramidal neurons.
Specific Modeling Methods
Mice: C57BL/6J • male • 7 weeks old • 22 g body weight
Administration: 10 μg in 5 μL • i.c.v.
Note
(1) The right lateral brain ventricle is localized with a stereotactic instrument.
(2) After the operation, skin was sutured, and keep the mice under a warming place until they wake up.
(3) 48 hours after lateral ventricle injection, the mice are anaesthetized using Isoflurane and then sequentially intracardially perfused with saline and PFA (4%, 30 mL). Rapidly remove The mouse brain processed for paraffin embedding or frozen sections.
Modeling Indicators
Electroencephalogram (EEG) recording: Had higher local maximal amplitude and reduced spike frequency compared to the control group.
Histology analysis: Showed Triangulated pyknotic nuclei and cytoplasmic shrinkage in the hippocampal neuron, and induced neuronal loss.
Opposite Product(s): Sitagliptin (HY-13749)

2. Induction of epilepsy model in rats[6]
Background
Kainic acid can bind to NMDA receptors which are abundant in neurons in the cornu ammonus of the hippocampus, amygdala, and pyriform cortex, and leading to variable levels of neuronal death in these regions.
Specific Modeling Methods
Rat: Sprague-Dawley rats • male
Administration: 10 mg/kg • i.p. • a single dose
Note
(1) Seizures occurres approximately 45 min after injection, typically lasted 2-3 hr.
(2) Kainic acid-treated animals may die during an acute period of intoxication, it's suggested to increase the number of animals per group.
(3) 72 hours later, the rats are anesthetized and immediately perfused transcardially with 50 mL 0.9% saline followed by 500 mL 0.1 m neutral phosphate-buffered formaldehyde (4%). And remove the brain and postfixed at 4°C overnight in the same fixative and dehydrated, embedded in paraffin, and cut into serial 6-μm-thick coronal sections at the level of the dorsal hippocampus.
Modeling Indicators
behavioral changes: Exhibited immobility and rigid postures firstly, followed by repetitive head nodding, ‘wet dog shakes’, and subsequent rearing and falling. Eventually, the rats developed generalized tonic-clonic seizures with continuous convulsions, lasting for several hours.
Histology analysis: Resulted in a loss of pyramidal neurons in fields CA1 and CA3 of the hippocampus.
Increaseed the size, arborization, and stainability of GFAP-immunoreactive cells.
Opposite Product(s): Melatonin (HY-B0075)

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