Kainic acid is a cyclic analog of L-glutamate and an agonist of ionotropic kainate receptors (KARs).
Specific subunits include KA1 (GluK4), KA2 (GluK5), GluR5 (GluK1), and GluR6 (GluK2). KARs are highly expressed in the hippocampus (especially CA3 pyramidal cells), amygdala, entorhinal cortex, basal ganglia, and cerebellum. [3]

海人酸能诱导神经元强烈去极化并最终导致细胞死亡，这是颞叶癫痫的核心现象。[3]
在非癫痫动物的海马脑切片中，浴槽应用KA可在CA3区诱导出高频伽马振荡（30-80 Hz）。[3]
在慢性癫痫小鼠（单侧海马注射KA后）的脑切片中，CA3区出现伽马活动，且树突抑制性OLM中间神经元的放电频率从theta频带转变为伽马频带。[3]
在体外，通过药物阻断海人酸受体可以抑制癫痫动物齿状回中的同步化网络驱动活动。[3]

海藻酸方案计划实施状况（5mg/kg；腹腔注射；至少一次至少三小时，配方方案连续状态）[1]。

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全身性、海马内或杏仁核内给予海人酸可诱导急性癫痫持续状态，其行为学特征包括面部阵挛、湿狗样抖动、前肢阵挛、站立和后仰跌倒等。[3]
初始SE之后，会有一个潜伏期（根据物种和给药途径不同，持续5-40天），之后出现自发性复发癫痫发作，模拟了人类颞叶癫痫的过程。[3]
KA给药会导致类似于人类TLE海马硬化的神经病理学改变，包括CA1/CA3/门区选择性神经元丢失、颗粒细胞弥散以及齿状回分子层异常的苔藓纤维出芽。[3]
海马体通常是癫痫发作的起始区，即使KA在远处部位（如杏仁核）给药也是如此，这表明海马在癫痫发作的产生和传播中起核心作用。[3]
脑电图特征包括发作间期棘波、伽马振荡（30-80 Hz）以及起源于海马或杏仁核的发作期放电。[3]
年龄影响易感性：非常年轻（P15以下）和年老的大鼠（P60及以上）对KA诱导的癫痫发作更敏感，与年轻成年大鼠（P20-P60）相比，SE潜伏期更短。未成熟大脑中的癫痫发作造成的神经元损伤较少，但可能导致GABA能信号传导的长期改变。[3]

Animal/Disease Models: 8 weeks, 200-250 g male adult Wistar rats[1]: 5 mg/kg
Route of Administration: intraperitoneal (ip) injection; at least 3 hrs (hrs (hours)) every hour until status epilepticus occurs.
Experimental Results: Induced epileptic seizures in rats.

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Systemic Administration (intraperitoneal, i.p.): In rats, a single dose of 6-15 mg/kg can induce status epilepticus (SE). Alternatively, multiple lower doses (e.g., 5 mg/kg/h) can be administered until SE occurs to reduce mortality. SE typically occurs about 1 hour after injection. Diazepam (20 mg/kg) and ketamine (50 mg/kg) can be used to terminate SE. Mortality rates range from 5% to 30%. [3]
Intrahippocampal Administration: In rats, doses ranging from 0.4 to 2.0 µg (in a small volume, e.g., 0.2 µL) are injected directly into the hippocampus. This induces convulsive SE within 5-60 minutes. Similar protocols are used in mice and guinea pigs. [3]
Intra-amygdaloid Administration: In rats, doses of 0.4–2 µg are injected into the amygdala, inducing acute seizures with symptoms similar to intrahippocampal injection, sometimes with additional signs like salivation and exophthalmos. In monkeys, doses of 0.5–10 µg/µl of saline are used, producing focal seizures with oral automatisms. [3]
Post-SE Monitoring: Following SE induction, animals enter a latent period. The development of chronic epilepsy is assessed via long-term video-EEG monitoring to detect spontaneous recurrent seizures. Neuropathological examination is performed at various time points after SE to assess neuronal damage. [3]

The provided text does not contain detailed pharmacokinetic data (e.g., absorption, distribution, metabolism, excretion, half-life, oral bioavailability) for kainic acid. [3]
It is noted that systemic administration offers no control over the bioavailability of KA in the brain. [3]
KA can enhance the permeability of the blood-brain barrier, an effect observed within 1 hour of administration and before SE onset. This increased permeability may lead to enhanced glutamate release in the hippocampus, favoring seizure occurrence. [3]

Mortality rates following systemic administration of kainic acid in rats range from 5% to 30%. [3]
KA is an excitotoxin. Its administration induces neuronal death, particularly in the CA3 and CA1 regions of the hippocampus, amygdala, and other limbic structures. The extent of damage correlates with the severity and propagation of seizure activity rather than solely direct toxin action. [3]
Age-specific toxicity is observed: young (P15) and old rats are more sensitive, showing shorter latency to SE and more severe seizures compared to young adults (P20-P60). Interestingly, in very young animals (less than 3 weeks), KA induces severe seizures but causes minimal brain damage, attributed to immature neural connectivity. [3]
Distant neuropathological changes (outside the injection site) are attributed to the propagation of epileptiform activity during SE, not to the direct neurotoxic effect of KA itself. Pretreatment with diazepam can prevent hippocampal damage from intra-amygdaloid KA without affecting local amygdala damage. [3]

[1]. Chronic levetiracetam decreases hippocampal and testicular aromatase expression in normal but not kainic acid-induced experimental model of acute seizures in rats. Neuroreport. 2017 Sep 27;28(14):903-909.

[2]. Kainic acid-mediated excitotoxicity as a model for neurodegeneration. Mol Neurobiol. 2005;31(1-3):3-16.

[3]. The kainic acid model of temporal lobe epilepsy. Neurosci Biobehav Rev. 2013 Dec;37(10 Pt 2):2887-99.

[4]. Scherer-Singler U, McGeer EG. Distribution and persistence of kainic acid in brain. Life Sci. 1979 Mar 12;24(11):1015-22.

[5]. The effect of dipeptidyl peptidase IV on disease-associated microglia phenotypic transformation in epilepsy. J Neuroinflammation. 2021 May 11;18(1):112.

[6]. Melatonin attenuates kainic acid-induced hippocampal neurodegeneration and oxidative stress through microglial inhibition. J Pineal Res. 2003 Mar;34(2):95-102.

Kainic acid is a dicarboxylic acid, a pyrrolidinecarboxylic acid, a L-proline derivative and a non-proteinogenic L-alpha-amino acid. It has a role as an antinematodal drug and an excitatory amino acid agonist. It is a conjugate acid of a kainate(1-).
Kainic acid has been reported in Digenea simplex, Apis cerana, and other organisms with data available.
(2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.

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Kainic acid was originally isolated from the red algae Digenea simplex and was initially intended as an ascaricide. [3]
It became a crucial tool in neuroscience for studying glutamate receptors, excitotoxicity, and for developing animal models of temporal lobe epilepsy (TLE). [3]
The KA model replicates key features of human TLE: a latent period after an initial injury (SE), spontaneous recurrent seizures, and hippocampal sclerosis. [3]
It is compared to other TLE models like pilocarpine and electrical kindling. The pilocarpine model is noted for high reliability in inducing epilepsy, while kindling allows controlled network targeting but rarely produces spontaneous seizures or hippocampal sclerosis. [3]
The choice between intracerebral and systemic KA administration depends on the research question: intracerebral for focal network studies, systemic for studying widespread vulnerability and disease. [3]
The model has contributed to understanding epileptogenesis, ictogenesis, and testing potential therapies. [3]

C10H15NO4.H2O

231.24568

213.1

487-79-6

Kainic acid hydrate;58002-62-3

10255

White to off-white solid powder

1.2±0.1 g/cm3

439.9±45.0 °C at 760 mmHg

253-254ºC

219.8±28.7 °C

0.0±2.3 mmHg at 25°C

1.509

0.5

86.63

3

5

4

15

300

3

CC(=C)[C@H]1CN[C@@H]([C@H]1CC(=O)O)C(=O)O

VLSMHEGGTFMBBZ-OOZYFLPDSA-N

InChI=1S/C10H15NO4/c1-5(2)7-4-11-9(10(14)15)6(7)3-8(12)13/h6-7,9,11H,1,3-4H2,2H3,(H,12,13)(H,14,15)/t6-,7+,9-/m0/s1

(2S,3S,4S)-3-(carboxymethyl)-4-prop-1-en-2-ylpyrrolidine-2-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~234.49 mM)
H2O : ~25 mg/mL (~117.24 mM)

配方 1 中的溶解度: ≥ 5 mg/mL (23.45 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 50.0 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 5 mg/mL (23.45 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 50.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 5 mg/mL (23.45 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 50.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。