The role of the nucleus basalis of Meynert and reticular thalamic nucleus in pathogenesis of genetically determined absence epilepsy in rats: A lesion study

Berdiev, R.K.; Chepurnov, S.A.; Veening, Jan G.; Chepurnova, N.E.; Luijtelaar, E.L.J.M. van

doi:10.1016/j.brainres.2007.09.010

Cited by 19 publications

(10 citation statements)

References 34 publications

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“…Systemic administration of scopolamine to healthy humans induces impairment to attentional processes, and memory, as well as decreases in higher frequency gamma/beta EEG power relative to lower frequency delta/theta power (Ebert and Kirch, 1998). Although not directly demonstrated in the current study, VNS has been shown to excite the nucleus basalis (NB) (Detari et al, 1983) and similarly to VNS, NB activation promotes arousal, suppresses seizure activity Berdiev et al, 2007), and promotes neural plasticity (Edeline et al, 1993;Engineer et al, 2011). The suppression of evoked responses to repetitive stimuli by brief activation of VNS we demonstrate are notably similar to the suppression induced by arousal (Castro-Alamancos and Connors, 1996b); however, their precise relationship remains unknown.…”

Section: Discussionmentioning

confidence: 55%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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Abstract-Vagus nerve stimulation (VNS) is an FDA approved treatment for drug-resistant epilepsy and depression.Recently, we demonstrated the capacity for repeatedly pairing sensory input with brief pulses of VNS to induce input specific reorganization in rat auditory cortex. This was subsequently used to reverse the pathological neural and perceptual correlates of hearing loss induced tinnitus. Despite its therapeutic potential, VNS mechanisms of action remain speculative. In this study, we report the acute effects of VNS on intra-cortical synchrony, excitability, and sensory processing in anesthetized rat auditory cortex. VNS significantly increased and decorrelated spontaneous multi-unit activity, and suppressed entrainment to repetitive noise burst stimulation at 6 -8 Hz but not after application of the muscarinic antagonist scopolamine. Collectively, these experiments demonstrate the capacity for VNS to acutely influence cortical synchrony and excitability and strengthen the hypothesis that acetylcholine and muscarinic receptors are involved in VNS mechanisms of action. These results are discussed with respect to their possible implications for sensory processing, neural plasticity, and epilepsy.

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Section: Discussionmentioning

confidence: 55%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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“…Lesions of the cholinergic nucleus basalis in GAERS suppressed SW discharges (Danober, Vergnes et al 1994) as well as the systemic administration of nicotine (Danober, Depaulis et al 1993). There were however contradictory results reported in WAG-Rij rats, with an increase of SW discharges after the selective removal of the cholinergic input from the nucleus basalis (Berdiev, Chepurnov et al 2007), and an inhibition of the corticothalamocortical synchronous activity related to cholinergic activation of the nucleus basalis, but mostly mediated via muscarinic receptors (Berdiev and van Luijtelaar 2009).…”

Section: A Potential Contribution Of Nachrs In the Process Of Ictogenmentioning

confidence: 93%

Nicotinic receptor abnormalities as a biomarker in idiopathic generalized epilepsy

Garibotto

Wissmeyer²,

Giavri³

et al. 2018

Eur J Nucl Med Mol Imaging

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Mutations of cholinergic neuronal nicotinic receptors have been identified in the autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), associated with changes on PET images using [ 18 F]-F-85380-A (F-A-85380), an α4β2 nicotinic receptor ligand. The aim of the present study was to evaluate potential changes in nicotinic receptor availability in other types of epilepsy. Methods: We included 34 male participants, 12 patients with idiopathic generalized epilepsy (IGE), 10 with non lesional diurnal focal epilepsy, and 12 age-matched healthy controls. All patients underwent PET/CT using F-A-85380 and [ 18 F]-fluorodeoxyglucose (FDG), 3D T1 MRI and diffusion tensor imaging (DTI). F-A-85380 and FDG images were compared with the control group using a voxel-wise (SPM12) and a volumes of interest (VOI) analysis. Results: In the group of patients with IGE, the voxel-wise and VOI analyses showed a significant increase of F-A-85380 ratio index of binding potential (BPRI, corresponding to the receptor availability) in the anterior cingulate cortex (ACC), without structural changes on MRI. At an individual level, F-A-85380 BPRI increase in the ACC could distinguish IGE patients from controls and from patients with focal epilepsy with good accuracy. Conclusions: We observed focal changes of density/availability of nicotinic receptors in IGE, namely an increase in the ACC. These data suggest that the modulation of α4β2 nicotinic receptors plays a role not only in ADNFLE but also in other genetic epileptic syndromes such as IGE and could serve as a biomarker of epilepsy syndromes with a genetic background.

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“…Nevertheless, the selective destruction of cholinergic cells within the NB provokes an increase of SWDs in the cortical EEG of adult WAG/Rij rats (Berdiev et al, 2007), suggesting that the activity of the cholinergic system indeed inhibits SWDs. Despite these data suggesting an involvement of the cholinergic system in seizure modulation, no specific studies on the central distribution or function of cholinergic receptors have so far been performed in this strain of rats.…”

Section: Acetylcholinementioning

confidence: 97%

“…It has been shown that mainly muscarinic cholinergic stimulation of the NB and, to a smaller extent, of the NRT, plays an important role in the inhibition of the CTC synchronous activity, typical for SWDs in WAG/Rij rats (Berdiev et al, 2007;Berdiev and van Luijtelaar, 2009). In particular, the administration of the cholinergic agonist carbachol in the NB suppressed SWD activity in WAG/Rij rats while the muscarinic antagonist scopolamine alone had no effect on SWDs, but antagonized the carbachol-induced decrease of cortical discharges (Berdiev and van Luijtelaar, 2009).…”

Section: Acetylcholinementioning

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 role of the nucleus basalis of Meynert and reticular thalamic nucleus in pathogenesis of genetically determined absence epilepsy in rats: A lesion study

Cited by 19 publications

References 34 publications

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Nicotinic receptor abnormalities as a biomarker in idiopathic generalized epilepsy

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

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