Effect of Vigabatrin on the Electroencephalogram in Rats

Halonen, Toivo; Pitkänen, Asla; Koivisto, Esa; Partanen, Juhani; Riekkinen, Paavo

doi:10.1111/j.1528-1157.1992.tb02294.x

Cited by 14 publications

(3 citation statements)

References 30 publications

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“…Long-standing reductions in GABAergic currents have been found in hippocampal slices obtained at P15-P17 from rats with recurrent flurothyl seizures during the first week of life (P0-P5) (Isaeva et al, 2006). The significantly faster theta frequency seen in the rats with recurrent seizures compared to the non-controls is another indication that inhibition was impaired in the recurrent seizure rats (Halonen et al, 1992). Since the interplay between principal cells and interneurons plays an important role in timing the activity of individual cells (Marshall et al, 2002), altered inhibition may also contribute to the deficits seen in the recurrent seizure rats.…”

Section: Discussionmentioning

confidence: 99%

Early life seizures cause long-standing impairment of the hippocampal map

Karnam

Zhou

Huang

et al. 2009

Experimental Neurology

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Children with seizures are at risk for long-term cognitive deficits. Similarly, recurrent seizures in developing rats are associated with deficits in spatial learning and memory. However, the pathophysiological bases for these deficits are not known. Hippocampal place cells, cells that are activated selectively when an animal moves through a particular location in space, provides the animal with a spatial map. We hypothesized that seizure-induced impairment in spatial learning is a consequence of the rat's inability to form accurate and stable hippocampal maps. To directly address the cellular concomitants of spatial memory impairment, we recorded the activity of place cells from hippocampal subfield CA1 in freely moving rats subjected to 100 brief flurothyl-induced seizures during the first weeks of life and then tested them in the Morris water maze and radial-arm water maze followed by place cell testing. Compared to controls, rats with recurrent seizures had marked impairment in Morris water maze and radial-arm water maze. In parallel, there were substantial deficits in action potential firing characteristics of place cells with two major defects: i) the coherence, information content, center firing rate, and field size were reduced compared to control cells; and ii) the fields were less stable than those in control place cells. These results show that recurrent seizures during early development are associated with significant impairment in spatial learning and that these deficits are paralleled by deficits in the hippocampal map. This study thus provides a cellular correlate for how recurrent seizures during early development lead to cognitive impairment.

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Section: Discussionmentioning

confidence: 99%

Early life seizures cause long-standing impairment of the hippocampal map

Karnam

Zhou

Huang

et al. 2009

Experimental Neurology

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“…Activity in the gamma band that is visible in EEG seizure recordings has been linked to impairment of dendritic GABAergic inhibition [82]. However, increasing GABA concentration by administrating the GABA antagonist vigibatrin has been shown to increase resting delta power in both rats [83] and humans [84], suggesting that a simple decrease in GABA does not fully explain the U-shaped spectral profile in ASD. For example, thalamocortical delta oscillations are produced by an interaction between GABAergic interneurons and N-methyl-D-aspartate receptors on glutamatergic neurons, which are in turn modulated by dopaminergic neurons in the thalamus [85].…”

Section: Reviewmentioning

confidence: 99%

Resting state EEG abnormalities in autism spectrum disorders

Wang

Barstein

Ethridge

et al. 2013

J Neurodevelop Disord

403

328

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Autism spectrum disorders (ASD) are a group of complex and heterogeneous developmental disorders involving multiple neural system dysfunctions. In an effort to understand neurophysiological substrates, identify etiopathophysiologically distinct subgroups of patients, and track outcomes of novel treatments with translational biomarkers, EEG (electroencephalography) studies offer a promising research strategy in ASD. Resting-state EEG studies of ASD suggest a U-shaped profile of electrophysiological power alterations, with excessive power in low-frequency and high-frequency bands, abnormal functional connectivity, and enhanced power in the left hemisphere of the brain. In this review, we provide a summary of recent findings, discuss limitations in available research that may contribute to inconsistencies in the literature, and offer suggestions for future research in this area for advancing the understanding of ASD.

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“…The neocortex contains different types of cells, such as the fast-rhythmic bursting neurons and fast spiking neurons which are capable to fire in a high frequent manner or in spike burst recurring at 30-50 Hz (Steriade, 2003). Furthermore, changes in GABAergic and Glutamatergic neurotransmission have been found to induce changes in spectral power of the EEG in these frequencies (Coenen and van Luijtelaar, 1989;Halonen et al, 1992;Lally et al, 2014). It remains therefore possible that different combinations of oscillation cells, each with their own firing and recurrent rates, permit each brain region to affect other parts of the brain within a unique combination of frequencies.…”

Section: Pre-ical Intra-cortical Network Changes and A 'Driving' Cortmentioning

confidence: 99%

Termination of ongoing spike-wave discharges investigated by cortico–thalamic network analyses

Lüttjohann

Schoffelen

Luijtelaar

2014

Neurobiology of Disease

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a b s t r a c t a r t i c l e i n f oPurpose: While decades of research were devoted to study generation mechanisms of spontaneous spike and wave discharges (SWD), little attention has been paid to network mechanisms associated with the spontaneous termination of SWD. In the current study coupling-dynamics at the onset and termination of SWD were studied in an extended part of the cortico-thalamo-cortical system of freely moving, genetic absence epileptic WAG/Rij rats. Methods: Local-field potential recordings of 16 male WAG/Rij rats, equipped with multiple electrodes targeting layer 4 to 6 of the somatosensory-cortex (ctx4, ctx5, ctx6), rostral and caudal reticular thalamic nucleus (rRTN & cRTN), ventral postero medial (VPM), anterior-(ATN) and posterior (Po) thalamic nucleus, were obtained. Six seconds lasting pre-SWD-N SWD, SWD-N post SWD and control periods were analyzed with timefrequency methods, and between-region interactions were quantified with frequency-resolved Granger Causality (GC) analysis. Results: Most channel pairs showed increases in GC lasting from onset to offset of the SWD. While for most thalamo-thalamic pairs a dominant coupling direction was found during the complete SWD, most corticothalamic pairs only showed a dominant directional drive (always from cortex to thalamus) during the first 500 ms of SWD. Channel pair ctx4-rRTN showed a longer lasting dominant cortical drive, which stopped 1.5 sec prior to SWD offset. This early decrease in directional coupling was followed by an increase in directional coupling from cRTN to rRTN 1 sec prior to SWD offset. For channel pairs ctx5-Po and ctx6-Po the heightened cortex-N thalamus coupling remained until 1.5 sec following SWD offset, while the thalamus-N cortex coupling for these pairs stopped at SWD offset. Conclusion: The high directional coupling from somatosensory cortex to the thalamus at SWD onset is in good agreement with the idea of a cortical epileptic focus that initiates and entrains other brain structures into seizure activity. The decrease of cortex to rRTN coupling as well as the increased coupling from cRTN to rRTN preceding SWD termination demonstrates that SWD termination is a gradual process that involves both cortico-thalamic as well as intrathalamic processes. The rostral RTN seems to be an important resonator for SWD and relevant for maintenance, while the cRTN might inhibit this oscillation. The somatosensory cortex seems to attempt to reinitiate SWD following its offset via its strong coupling to the posterior thalamus.© 2014 Elsevier Inc. All rights reserved. IntroductionAbsence epilepsy (AE) is a neurological disorder, mostly found in young children, which is characterized by frequent, spontaneously starting and spontaneously stopping, lapses of consciousness. The major electrophysiological characteristic of AE are the spontaneously starting and stopping, rhythmic, generalized, bilateral synchronous spike and wave discharges (SWD), which are known to be generated within the cortico-thalamo-cortical system (Depaulis and v...

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Effect of Vigabatrin on the Electroencephalogram in Rats

Cited by 14 publications

References 30 publications

Early life seizures cause long-standing impairment of the hippocampal map

Early life seizures cause long-standing impairment of the hippocampal map

Resting state EEG abnormalities in autism spectrum disorders

Termination of ongoing spike-wave discharges investigated by cortico–thalamic network analyses

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