Specific alteration in the expression of glial fibrillary acidic protein, glutamate dehydrogenase, and glutamine synthetase in rats with genetic absence epilepsy

Dutuit, Magali; Didier-Bazes, M.; Vergnes, Marguerite; Mutin, M; Conjard, Agnès; Akaoka, H.; Belin, Marie‐Françoise; Touret, Monique

doi:10.1002/1098-1136(200010)32:1<15::aid-glia20>3.0.co;2-#

Cited by 68 publications

(46 citation statements)

References 59 publications

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“…However, it was demonstrated that the LPS evoked increase in pro-inflammatory cytokines can increase absence epileptic activity between 30 and 270 min after injection independently from inflammation induced body temperature changes (Kovács et al, 2006(Kovács et al, , 2011, in which IL-1␤ may be one of the main pro-epileptic (pro-absence) mediators possibly via GABAergic neurotransmission (Van Luijtelaar et al, 2012) in WAG/Rij animals. Nevertheless, the presence of reactive astrocytes in the GAERS cortex and thalamus before the onset of absence epileptic seizures (Dutuit et al, 2000) and IL-1␤ induction in reactive astrocytes of adult GAERS rat somatosensory cortex at the onset of SWDs and the contribution of IL-1␤ to SWD occurrence were also demonstrated in GAERS rats (Akin et al, 2011). Thus, we can conclude that pro-inflammatory cytokines may have aggravating influence on absence epileptic activity (genesis and recurrence of SWDs) at least in the investigated two rat models (WAG/Rij, GAERS) of absence epilepsy and also in Long Evans rats.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induced increase in seizure activity in two animal models of absence epilepsy WAG/Rij and GAERS rats and Long Evans rats

Kovács

Dobolyi

Juhász

et al. 2014

Brain Research Bulletin

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Absence epileptic rats a b s t r a c tWe showed previously that the number and time of spike-wave discharges (SWDs) were increased after intraperitoneal (i.p.) injection of lipopolysaccharide (LPS), an effect, which was completely abolished by cyclooxygenase-2 (COX-2) inhibitor indomethacin (IND) pretreatment in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats. These and other results suggest that injection of LPS to genetically absence epileptic animals, such as WAG/Rij rats, may allow us to investigate relationships between absence epilepsy and LPS evoked neuroinflammation processes. However, LPS may evoke different effects on absence epileptic activity in various animal strains. Thus, to extend our previous results, we injected two doses of LPS (50 g/kg and 350 g/kg i.p.) alone and in combination with IND (10 mg/kg IND i.p. +50 g/kg LPS) into rats of two model animal strains (WAG/Rij rats; GAERS rats: Genetic Absence Epileptic Rats from Strasbourg) and into Long Evans rats. The effects of treatments on SWD number and SWD duration were examined. Both doses of LPS increased the SWD number and the total time of SWDs dose-dependently during the whole 4-h recording period, which was abolished by IND pretreatment in all three investigated strains. These results extend our previous results suggesting that our methods using LPS injection into freely moving absence epileptic rats is applicable not only in well-established animal models of absence epilepsy such as WAG/Rij rats and GAERS rats but also in Long Evans rats to investigate links between inflammation and absence epilepsy.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induced increase in seizure activity in two animal models of absence epilepsy WAG/Rij and GAERS rats and Long Evans rats

Kovács

Dobolyi

Juhász

et al. 2014

Brain Research Bulletin

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“…Interestingly, in a rat model for generalized epilepsy, an increase in astrocyte GDH expression was identified before the onset of epilepsy. 34 HI/HA patients with seizures did have GDH mutations associated with significant impairments in GTP inhibition of GDH. However, the absence of persistent seizures in patients with similar enzymatic study results and the disparity between HI/HA-affected family members argues against a simple genotype-phenotype correlation.…”

Section: Mechanism Of Epilepsy In Hi/ha Patientsmentioning

confidence: 90%

Central nervous system hyperexcitability associated with glutamate dehydrogenase gain of function mutations

Raizen¹,

Brooks‐Kayal²,

Steinkrauss³

et al. 2005

The Journal of Pediatrics

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“…Dutuit et al (2000) demonstrated that expression of glial fibrillary acidic protein (GFAP), the first sign of reactive astrocytosis, and its mRNA levels were increased in the cortex and thalamus of both adult and young GAERS suggesting that reactive astrocytes are present before the development of absence seizures (Dutuit et al, 2000). Therefore, reactive astrocytes, already present before the onset of seizures, might contribute to the processes giving rise to epileptic seizures by modifying relevant neuronal structures.…”

Section: Glia Neuroinflammation and The Mtor Pathwaymentioning

confidence: 99%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

128

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Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development.Neuroscience and Biobehavioral Reviews http://dx.doi.org/10. 1016/j.neubiorev.2016.09.017 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 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. AbstractThe WAG/Rij rat model has recently gathered attention as a suitable animal model of absence epileptogenesis. This latter term has a broad definition encompassing any possible cause that determines the development of spontaneous seizures; however, most of, if not all, preclinical knowledge on epileptogenesis is confined to the study of post-brain insult models such as traumatic brain injury or post-status epilepticus models. WAG/Rij rats, but also synapsin 2 knockout, Kv7 current-deficient mice represent the first examples of genetic models where an efficacious antiepileptogenic treatment (ethosuximide) was started before seizure onset. In this review, we have critically reconsidered all articles published regarding WAG/Rij rats, from the perspective that the period before SWD onset is considered as the latent period. In our new theory on seizure development, it is proposed that genes might be considered as the initial "insult" responsible for all plastic changes underpinning the development of spontaneous seizures. According to this idea, in WAG/Rij rats, genetic predisposition would lead to the development of abnormal bilateral cortical epileptic foci, which would then nongenetically stimulate the rest of the brain to rearrange networks in order to phenotypically develop seizures similarly to what happens during electrical kindling.

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Specific alteration in the expression of glial fibrillary acidic protein, glutamate dehydrogenase, and glutamine synthetase in rats with genetic absence epilepsy

Cited by 68 publications

References 59 publications

Lipopolysaccharide induced increase in seizure activity in two animal models of absence epilepsy WAG/Rij and GAERS rats and Long Evans rats

Lipopolysaccharide induced increase in seizure activity in two animal models of absence epilepsy WAG/Rij and GAERS rats and Long Evans rats

Central nervous system hyperexcitability associated with glutamate dehydrogenase gain of function mutations

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

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