Injections of kainic acid into the amygdaloid complex of the rat: An electrographic, clinical and histological study in relation to the pathology of epilepsy

Ben‐Ari, Yehezkel; Tremblay, E.; Ottersen, Ole Petter

doi:10.1016/0306-4522(80)90049-4

Cited by 349 publications

(136 citation statements)

References 28 publications

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“…Commonly, the systemic or intracerebral injections of chemical convulsants such as pilocarpine or kainic acid have been used (Ben-Ari et al, 1980;Cavalheiro et al, 1982;Turski et al, 1983). Also, prolonged stimulation of the hippocampus and other limbic regions with implanted electrodes has been used to produce self-sustaining SE (McIntyre et al, 1982;Brandt et al, 2003).…”

Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

258

286

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

258

286

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“…On the day before the kainic acid injection, the baseline EEG was recorded for 12 h. On the morning of the first day thereafter, the animals were given a single intra-amygdaloid injection of kainic acid (750 ng) (Ben-Ari et al, 1980;Berger et al, 1986) during the period of EEG and video recording. An infusion cannula (C315I; Plastics One) with a polyethylene tube extension (PE 20) was put into the guide cannula and fixed by a captive collar of the external tube to allow injections to be made in freely moving rats.…”

Section: Experimental Protocolmentioning

confidence: 99%

Intra-Amygdaloid Injection of Kainic Acid in Rats with Genetic Absence Epilepsy: The Relationship of Typical Absence Epilepsy and Temporal Lobe Epilepsy

Gurbanova¹,

Aker²,

Şirvancı³

et al. 2008

J. Neurosci.

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We showed previously that genetic absence epilepsy rats from Strasbourg (GAERS) resist secondary generalization of focal limbic seizures after electrical kindling. We now investigate the effect of intra-amygdaloid injection of kainic acid, as another model of temporal lobe epilepsy, focusing on epileptogenesis, spike-and-wave discharges (SWDs), and the transition from basal to SWD states in GAERS. The EEG was recorded from the hippocampus and cortex of adult GAERS and Wistar rats before kainic acid injections into the basolateral amygdala and for 3 months thereafter. EEG and video recordings monitored SWDs and convulsive seizures. We analyzed spectral changes of the EEG during kainic acid-induced status epilepticus, SWDs, for 10 s before (silent period) and for 2 s before (transition period) SWDs. After the injection of kainic acid, all animals experienced convulsive seizures for at least 3 h. The first convulsive seizure was significantly delayed in GAERS compared with Wistar rats. SWDs and increases in power of the delta, alpha, and beta frequency ranges during the transition period disappeared after the kainic acid injection for 1-3 d and gradually reappeared. Power increases in the delta and alpha ranges were significantly correlated with the number of SWDs, in the beta and alpha ranges with their mean duration. Neo-Timm's staining at the end of experiments demonstrated that mossy fiber sprouting in GAERS is less pronounced than in Wistar rats. Our findings show that mechanisms underlying absence epilepsy and temporal lobe epilepsy interact with each other, although a site of this interaction remains to be defined.

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“…Studies using KA have provided major contributions to the understanding of neuronal cell death caused by excitotoxicity. Administration of KA is known to induce a sequence of altered behavioral events characterized by epileptiform seizures (Ben-Ari et al 1980, Sperk 1994, which are followed by neurodegeneration in specific brain regions, such as the hippocampus, piriform cortex, thalamus, and amygdala. In the hippocampus, the CA3 pyramidal cells and interneurons in the hilus of the dentate gyrus are the most vulnerable, followed by CA1 pyramidal cells (Coyle 1983, Sperk et al 1985, Tauck & Nadler 1985.…”

Section: Introductionmentioning

confidence: 99%

Ghrelin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

Lee¹,

Lim²,

Kim³

et al. 2010

Journal of Endocrinology

105

111

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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 a, interleukin-1b, 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.

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Injections of kainic acid into the amygdaloid complex of the rat: An electrographic, clinical and histological study in relation to the pathology of epilepsy

Cited by 349 publications

References 28 publications

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Intra-Amygdaloid Injection of Kainic Acid in Rats with Genetic Absence Epilepsy: The Relationship of Typical Absence Epilepsy and Temporal Lobe Epilepsy

Ghrelin attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

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