Spontaneous motor seizures of rats with kainate-induced epilepsy: effect of time of day and activity state

Hellier, Jennifer L.; Dudek, F. Edward

doi:10.1016/s0920-1211(98)00127-2

Cited by 96 publications

(97 citation statements)

References 25 publications

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“…In order to determine when during the cycle to carry out observations, a 24-h observation period was scheduled. Based on the results obtained and those of others [23], subsequent observations were done during the light-phase of the cycle. Figure 6 for experimental design) Kainic Acid Treatment: Rats (n = 147) received ip injections of KA (5 mg/kg/h) dissolved in physiological saline, over the course of 4 h or until two, stage-V seizures were presented by the animal.…”

Section: Experiments 1: Effect Of Ka Treatment (See Figure 4 For Expermentioning

confidence: 86%

“…Systemic administration of repeated, low doses of KA, results in a pattern of hippocampal degeneration similar to that observed after a single, high dose of kainate, with improved survival, and increased percentage of animals showing spontaneous seizures [20,23,24,33]. After KA administration, during the acute phase that may last up to 10 hours, the animal presents immobility, facial clonus, sniffing, wet dog shakes, and stage III to V seizures (rated according to Racine's scale), all leading to status epilepticus (SE).…”

Section: Introductionmentioning

confidence: 86%

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Intranigral transplants of a GABAergic cell line produce long-term alleviation of established motor seizures

Castillo

Mendoza-Trejo

Aguilar

et al. 2008

Behavioural Brain Research

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We have previously shown that intranigral transplants of immortalized GABAergic cells decrease the number of kainic acid-induced seizures [5] in an animal model. In the present study, recurrent NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript spontaneous behavioral seizures were established by repeated systemic injections of this excitotoxin into male Sprague Dawley rats. After the seizures had been established, cells were transplanted into the substantia nigra. Animals with transplants of control cells (without hGAD67 expression) or with sham transplants showed a death rate of more than 40% over the 12 weeks of observation, whereas in animals with M213-2O Cl4 transplants, the death rate was reduced to less than 20%. The M213-2O Cl4 transplants significantly reduced the percentage of animals showing behavioral seizures; animals with these transplants also showed a lower occurrence of stage V seizures than animals in the other groups. In vivo and in vitro analyses provided evidence that the GABAergic cells show sustained expression of both GAD67 and hGAD67cDNA, as well as increased GABA levels in the ventral mesencephalon of transplanted animals. Therefore, transplantation of GABA-producing cells can produce long-term alleviation of behavioral seizures in an animal model.

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Section: Experiments 1: Effect Of Ka Treatment (See Figure 4 For Expermentioning

confidence: 86%

Section: Introductionmentioning

confidence: 86%

Intranigral transplants of a GABAergic cell line produce long-term alleviation of established motor seizures

Castillo

Mendoza-Trejo

Aguilar

et al. 2008

Behavioural Brain Research

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show abstract

“…Daily variation in the frequency and severity of epileptic seizures in animal models has been described for kainic acid [27]-and pilocarpine [28]-induced motor seizures, and recently in AY-induced atypical absence seizures [29]. The purported involvement of the hippocampal formation in each of these seizure models suggests that its connectivity with the suprachiasmatic nucleus (SCN) [30], a region of the hypothalamus that regulates the expression of physiological and behavioral events in response to environmental time cues [31], may form the substrate for circadian rhythmicity in seizure activity.…”

Section: Discussionmentioning

confidence: 99%

Circadian distribution of generalized tonic–clonic seizures associated with murine succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism

Stewart

Nylen

Persinger

et al. 2008

Epilepsy & Behavior

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Human succinic semialdehyde dehydrogenase (SSADH) deficiency is an autosomal recessive disorder of GABA metabolism associated with motor impairment and epileptic seizures. Similarly, mice with targeted deletion of the Aldh5a1 gene (Aldh5a1 −/− ) exhibit SSADH deficiency and seizures early in life. These seizures begin as absence seizures the second week of life, but evolve into generalized convulsive seizures that increase in severity and become lethal during the fourth postnatal week. The seizures are alleviated and survival is prolonged when the mutant animals are weaned onto a ketogenic diet (KD). The persistence of spontaneous, recurrent, generalized tonic-clonic seizures in KD-treated adult Aldh5a1 −/− mice allowed us to quantify their daily (circadian) distribution using a novel behavioral method based on the detection of changes in movement velocity. Adult KD-treated Aldh5a1 −/− mice exhibited a seizure phenotype characterized by fits of wild running clonus accompanied by jumping and bouncing. These hypermotor seizures were largely spontaneous and occurred daily in a nonrandom pattern. The seizure rhythm showed a peak shortly after dark phase onset (2008 hours) with near-24-hour periodicity. Age-matched wild-type littermates showed no evidence of abnormal motor behavior. These new data suggest that generalized tonicclonic seizures in Aldh5a1 −/− mice are more frequent during a specific time of day and will provide useful information to clinicians for the treatment of seizures associated with human SSADH deficiency.

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“…Status epilepticus procedures were adapted from previous reports and were based on a model of chronic temporal lobe epilepsy that yields a low mortality rate (Hellier et al, 1998;Hellier & Dudek, 1999;Hattiangady et al, 2004). Kainic acid (KA) was obtained from Ocean Produce International (Shelburne, Nova Scotia, Canada) and was dissolved in 0.9% sterile saline (Sigma, St. Louis, MO).…”

Section: Induction Of Status Epilepticus and Bromodeoxyuridine Injectmentioning

confidence: 99%

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

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Prenatal choline supplementation (SUP) protects adult rats against spatial memory deficits observed after excitotoxin-induced status epilepticus (SE). To examine the mechanism underlying this neuroprotection, we determined the effects of SUP on a variety of hippocampal markers known to change in response to SE and thought to underlie ensuing cognitive deficits. Adult offspring from rat dams that received either a Control or SUP diet on embryonic days 12-17 were administered saline or kainic acid (i.p.) to induce SE and were euthanized 16 days later. SUP markedly attenuated seizure-induced hippocampal neurodegeneration, dentate cell proliferation, hippocampal GFAP mRNA expression levels, prevented the loss of hippocampal GAD65 protein and mRNA expression, and altered growth factor expression patterns. SUP also enhanced pre-seizure hippocampal levels of BDNF, NGF, and IGF-1, which may confer a neuroprotective hippocampal microenvironment that dampens the neuropathological response to and/or helps facilitate recovery from SE to protect cognitive function. Keywords choline; kainic acid; hippocampus; seizures; bromodeoxyuridine; growth factor; glutamic acid decarboxylase; glial fibrillary acidic protein; neuroprotection Status epilepticus (SE), a period of prolonged seizures, produces a host of plastic changes in the hippocampus that are thought to contribute to the development of temporal lobe epilepsy. SE results in substantial neuronal loss (Cavazos et al., 1994;Haas et al., 2001;Gorter et al., 2003), γ-aminobutyric acid (GABA) system alterations (e.g., Houser & Esclapez, 1996), reactive gliosis (Jorgensen et al. 1993; Niquet et al., 1994a;Kang et al., 2006), mossy fiber innervation of the dentate gyrus (Sutula et al., 1988;Ben-Ari & Represa, 1990), changes in levels of growth factors (Khrestchatisky et al., 1995;Mudo et al., 1996;Schmidt-Kastner et al., 1996;Shetty et al., 2004), and a transient increase in cell proliferation and neurogenesis (Bengzon et al., 1997;Parent et al., 1997;Scharfman et al., 2000;Hattiangady et al., 2004). These SE-induced degenerative and regenerative changes in the hippocampus are also Corresponding author: Dr. Christina L. Williams, Department of Psychology and Neuroscience, 572 Research Drive, Box 91050, GSRB-II, Room 3022, Duke University, Durham, NC 27708, USA, Phone: 919-660-5638, Fax: 919-660-5798, Email: williams@psych.duke.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. accompanied by deficits in hippocampal-dependent learning and memory (Stafstrom et al., 1993;Liu et al., 1994;Sarkisian et al., 1997;Hort et al., 1999;Mik...

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Spontaneous motor seizures of rats with kainate-induced epilepsy: effect of time of day and activity state

Cited by 96 publications

References 25 publications

Intranigral transplants of a GABAergic cell line produce long-term alleviation of established motor seizures

Intranigral transplants of a GABAergic cell line produce long-term alleviation of established motor seizures

Circadian distribution of generalized tonic–clonic seizures associated with murine succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

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