The preferential mGlu2/3 receptor antagonist, LY341495, reduces the frequency of spike–wave discharges in the WAG/Rij rat model of absence epilepsy

Ngomba, Richard Teke; Biagioni, Francesca; Casciato, Sara; Bree, P.C.M. Willems-van; Battaglia, Giuseppe; Bruno, Valeria; Nicoletti, Ferdinando; Luijtelaar, E.L.J.M. van

doi:10.1016/j.neuropharm.2005.05.019

Cited by 54 publications

(45 citation statements)

References 81 publications

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“…van Luijtelaar and Coenen, 1988;Ngomba et al, 2005). The OSDS was able to detect SWDs with a mean sensitivity as high as 100% and a mean precision of 96.9% (range 94.3-100%) in our data set of eight different ECoG recordings (n = 8) of 5 h (see Table 1 for details).…”

Section: Resultsmentioning

confidence: 66%

An algorithm for real-time detection of spike-wave discharges in rodents

Ovchinnikov

Lüttjohann

Hramov

et al. 2010

Journal of Neuroscience Methods

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Section: Resultsmentioning

confidence: 66%

An algorithm for real-time detection of spike-wave discharges in rodents

Ovchinnikov

Lüttjohann

Hramov

et al. 2010

Journal of Neuroscience Methods

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“…MGlu2/3 receptors are preferentially localized on presynaptic nerve terminals, where they negatively modulate both glutamate and GABA release. 60 The putative role of some of the metabotropic glutamate (mGlu2/3, mGlu4, and mGlu1) receptors in the somatosensory cortex was investigated with a comparison between presymptomatic (2-3 months) and symptomatic (6-8 months) WAG/Rij's and ACI's. A recent study showed that there were no differences between presymptomatic and symptomatic WAG/Rij and aged matched ACI rats in the mRNA levels of cortical mGlu1 receptors, as determined by in situ hybridization.…”

Section: Changes In Membrane Properties Of Neurons In the Neocorticalmentioning

confidence: 99%

On the Origin and Suddenness of Absences in Genetic Absence Models

2011

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The origin of spike-wave discharges (SWDs), typical for absences, has been debated for at least half a century. While most classical views adhere to a thalamic oscillatory machinery and an active role of the cortex in modifying normal oscillations into pathological SWDs, recent studies in genetic models such as WAG/Rij and GAERS rats have challenged this proposal. It seems now well established that SWDs originate from the deep layers of the somatosensory cortex, that the activity quickly spreads over the cortex and invades the thalamus. The reticular thalamic nucleus and other thalamic nuclei provide a resonance circuitry for the amplification, spreading and entrainment of the SWDs. Conclusive evidence has been found that the changed functionality of HCN1 channels is a causative factor for the changes in local excitability and age-dependent increase in SWD. Furthermore, upregulation of two subtypes of Na+ channels, reduction of GABAB and mGlu 2/3 receptors might also play a role in the local increased excitability in WAG/Rij rats. Signal analytical studies have also challenged the view that SWDs occur suddenly from a normal background EEG. SWDs are recruited cortical responses and they develop from increasing associations within and between cortical layers and subsequently subcortical regions, triggered by the simultaneous occurrence of theta and delta precursor activity in the cortex and thalamus in case both structures are in a favorable condition, and increased directional coupling between cortex and thalamus. It is hypothesized that the cortex is the driving force throughout the whole SWD and is also responsible for its end.

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“…Instead, no changes in mGlu2/3 receptors expression and function were found in pre-seizure 2-months-old WAG/Rij rats. Pharmacological blockade of mGlu2/3 receptors with LY341495 reduces and treatment with a selective mGlu2/3 receptor agonist (LY379268) increases the incidence of SWDs in WAG/Rij rats (Ngomba et al, 2005). mGlu2/3 receptors are involved in absence seizures in this strain; the up-regulation of these receptors in the somatosensory cortex and other areas being evident only in adult epileptic rats indicates that this might be a consequence of repetitive seizures or an epiphenomenon.…”

Section: Group-ii (Mglu2/3 Receptors)mentioning

confidence: 84%

“…Epileptic 6-month-old WAG/Rij rats have an increased expression of mGlu2/3 receptors in the ventrolateral portion of the somatosensory cortex, which includes the putative "triggering zone(s)" of SWDs (Meeren et al, 2002;Ngomba et al, 2005). The expression of these receptors is also increased in ventrobasal thalamic nuclei and in the hippocampus, but not in the NRT.…”

Section: Group-ii (Mglu2/3 Receptors)mentioning

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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The preferential mGlu2/3 receptor antagonist, LY341495, reduces the frequency of spike–wave discharges in the WAG/Rij rat model of absence epilepsy

Cited by 54 publications

References 81 publications

An algorithm for real-time detection of spike-wave discharges in rodents

An algorithm for real-time detection of spike-wave discharges in rodents

On the Origin and Suddenness of Absences in Genetic Absence Models

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

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