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Focal limbic seizures induced by kainic acid: effects of bilateral subthalamic nucleus stimulation
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Andrew Pan, Atthaporn Boongird, Takaheru Kunieda, Imad Najm, Hans O Lüders
Kainic acid (KA) has been injected directly into the subcutaneous tissue, veins, peritoneum, hippocampus, amygdala and into the ventricles to induce seizures.1,3–13 The systemic or focal administration of KA induces distinct clinical seizure stages.1,13–15 Within the first 20–30 minutes, animals exhibit decreased activity, ‘staring’, drooling, followed by head nodding, ‘wet dog shakes’ lasting 30–60 minutes. Approximately an hour post-injection, recurrent seizures that are characterized by masticatory or facial movements, tremor of the forepaws, rearing and loss of postural tone ensue. These seizures increase in intensity, duration and occur at progressively shorter interictal periods. This is followed by almost continuous convulsions, lasting up to 2–5 hours. The surviving animals (up to 30% mortality) return to ‘normal’ for a silent period of between 5 and 21 days before up to half to almost all animals begin to exhibit spontaneous (or during handling), recurrent limbic seizures.15,16 Recurrent injections of kainic acid lead to more severe clinical seizures.9
Causes Of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Another example is the vulnerability of neurons to systemic kainic acid, a toxic substance derived from seaweed. Those neurons that possess high densities of membrane receptors for kainic acid die after systemic exposure to the compound. When injected directly into the brain, kainic acid is toxic to most neurons because most neurons have a few kainate receptors, and the compound is extremely toxic.
Experimental Models of Status Epilepticus
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
The kainic acid model of SE is one of the most extensively studied seizure models. It is regularly used to induce SE and shares many of the features of human temporal lobe epilepsy (TLE).11 Kainic acid, an extract of the seaweed Digenea simplex,27 is a rigid analog of glutamate that binds to a subset of glutamate receptors. Kainic acid was originally used as a lesioning agent because it kills cell bodies of neurons but spares glia and axons passing through the injection site.28-30 When the brains from kainic acid-injected animals are examined, additional damage is found in brain regions distant to the injection site.31 This suggests there are two mechanisms by which kainic acid induces neuronal damage, a direct excitotoxic effect and seizure-induced damage at a distance from the injection site. The distant damage is likely due to the synaptic release of glutamate secondary to kainic acid-induced seizure activity.31,32
Protein transduction domain of translationally controlled tumor protein: characterization and application in drug delivery
Published in Drug Delivery, 2022
Treatment with paraquat induces intracellular generation of superoxide anion and subsequent cell damage by oxidative stress (McCarthy et al., 2004). TAT-SOD showed better efficiency than TCTP-SOD although both complexes protected the cells from the paraquat-induced cell cytotoxicity in SH-SY5Y cells (Lee et al., 2011). Following intraperitoneal injection of TCTP-SOD and TAT-SOD in mice, both were delivered to the hippocampal region of the brain and protected brain cells from kainic acid-induced neuronal damage. Kainic acid, a cyclic analog of L-glutamate, is a potent neuroexcitatory agent that binds to glutamate receptor and induces an influx of calcium into cytoplasm, followed by the activation of free radical-generating enzymes (Coyle & Puttfarcken, 1993), eventually resulting in brain damage. Of note, TCTP-SOD showed more extensive distribution in the hippocampal region and enhanced protection from neuronal deaththan that of TAT-SOD (Lee et al., 2011), indicating an efficient translocating ability of TCTP-PTD through the blood brain barrier (BBB).
Neuronal protective effect of Songling Xuemaikang capsules alone and in combination with carbamazepine on epilepsy in kainic acid-kindled rats
Published in Pharmaceutical Biology, 2019
Haiyan Yang, Rui Zhang, Chen Jia, Mengyu Chen, Wen Yin, Liming Wei, Haisheng Jiao
All of the rats were anaesthetized with 10% chloral hydrate intraperitoneally (0.35 g/kg body weight) and fixed into a stereotaxic apparatus (Brain Stereotaxic Instrument, RWD Life Science Co., Ltd., China). The dorsal surface of the skull was exposed with a midline incision. Based on the stereotaxic atlas, a burr hole was drilled at the following location (coordinates from the bregma: anterior-posterior = −0.85 mm, lateral = −1.90 mm, ventral = −5.5 mm). The SD rats were randomly divided into five groups (n = 14): a control group, a CBZ group, a SXC group, a combination group of SXC + CBZ and a saline sham-operated group. The first four groups were injected with 0.45 μL kainic acid slowly over 10 min (1.0 μg/μL, #K0250; Sigma-Aldrich, St. Louis, MO), whereas the saline group was injected with normal saline. All surgeries were performed under anaesthesia with chloral hydrate and efforts were made to minimize animal suffering. Additional care was taken the days following an operation by providing the animals with comfortable space and enriched soft food.
Oxidative stress in epilepsy
Published in Expert Review of Neurotherapeutics, 2018
Ursula Geronzi, Federica Lotti, Salvatore Grosso
The use of appropriate animal models is essential to understand the complex mechanisms underlying epileptogenesis. Some of the most frequently used models of epilepsy are based on the use of chemoconvulsants, such as pilocarpine and kainic acid. Kainic acid is an L-glutamate analog which causes neuronal depolarization and seizures preferentially targeting the hippocampus. Pilocarpine is a muscarinic acetylcholine receptor agonist which is able to induce a status epilepticus. Other compounds include pentylenetetrazol, strychnine, N-methyl-D,L-aspartate, and dl-homocysteic acid and quinolinic acid, which are endogenous agonists of NMDA receptor [10]. Another type of animal model is represented by electroclinical stimulation. In particular, kindling is the most studied model of electroclinical stimulation. It refers to a seizure-induced plasticity phenomenon that occurs when repeated electroclinical stimulations in specific brain regions evoke progressive enhancement of seizure susceptibility [10]. All these models intend to mimic human epilepsy; therefore, mice usually show a similar clinical history as the human counterpart, presenting generalized as well focal epilepsies. Experimental models are also divided into acute (reactive or provoked), in which a seizure is induced by electrical or chemical stimulation in naïve, healthy, non-epileptic animals, and chronic, which are models using animals being made epileptic by electroclinical or chemical means or using animals with inborn epilepsy [10].