Literature DB >> 11896171

Activity of thalamic reticular neurons during spontaneous genetically determined spike and wave discharges.

Sean J Slaght1, Nathalie Leresche, Jean-Michel Deniau, Vincenzo Crunelli, Stephane Charpier.   

Abstract

This study reports the first intracellular recordings obtained during spontaneous, genetically determined spike and wave discharges (SWDs) in nucleus reticularis thalami (NRT) neurons from the genetic absence epilepsy rats from Strasbourg (GAERS), a model that closely reproduces the typical features of childhood absence seizures. A SWD started with a large hyperpolarization, which was independent of the preceding firing, and decreased in amplitude but did not reverse in polarity up to potentials >/= -90 mV. This hyperpolarization and the slowly decaying depolarization that terminated a SWD were unaffected by recording with KCl-filled electrodes. The prolonged (up to 15 action potentials), high-frequency bursts present during SWDs were tightly synchronized between adjacent neurons, correlated with the EEG spike component, and generated by a low-threshold Ca(2+) potential, which, in turn, was brought about by the summation of high-frequency, small-amplitude depolarizing potentials. Fast hyperpolarizing IPSPs were not detected either during or in the absence of SWDs. Recordings with KCl-filled electrodes, however, showed a more depolarized resting membrane potential and a higher background firing, whereas the SWD-associated bursts had a longer latency to the EEG spike and a lower intraburst frequency. This novel finding demonstrates that spontaneous genetically determined SWDs occur in the presence of intra-NRT lateral inhibition. The unmasking of these properties in the GAERS NRT confirms their unique association with spontaneous genetically determined SWDs and thus their likely involvement in the pathophysiological processes of the human condition.

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Year:  2002        PMID: 11896171      PMCID: PMC6758255     

Source DB:  PubMed          Journal:  J Neurosci        ISSN: 0270-6474            Impact factor:   6.167


  52 in total

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4.  On the putative contribution of GABA(B) receptors to the electrical events occurring during spontaneous spike and wave discharges.

Authors:  S Charpier; N Leresche; J M Deniau; S Mahon; S W Hughes; V Crunelli
Journal:  Neuropharmacology       Date:  1999-11       Impact factor: 5.250

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Authors:  M Steriade; F Amzica; D Neckelmann; I Timofeev
Journal:  J Neurophysiol       Date:  1998-09       Impact factor: 2.714

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Authors:  O C Snead
Journal:  Eur J Pharmacol       Date:  1992-03-31       Impact factor: 4.432

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  46 in total

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Review 2.  A brief history on the oscillating roles of thalamus and cortex in absence seizures.

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Journal:  Epilepsia       Date:  2012-02-23       Impact factor: 5.864

3.  Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy.

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4.  Reticular nucleus-specific changes in alpha3 subunit protein at GABA synapses in genetically epilepsy-prone rats.

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Journal:  Proc Natl Acad Sci U S A       Date:  2007-07-13       Impact factor: 11.205

5.  A gain in GABAA receptor synaptic strength in thalamus reduces oscillatory activity and absence seizures.

Authors:  Claude M Schofield; Max Kleiman-Weiner; Uwe Rudolph; John R Huguenard
Journal:  Proc Natl Acad Sci U S A       Date:  2009-04-20       Impact factor: 11.205

6.  Extrasynaptic GABA(A) receptors couple presynaptic activity to postsynaptic inhibition in the somatosensory thalamus.

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Journal:  J Neurosci       Date:  2013-09-11       Impact factor: 6.167

7.  Intracellular activity of cortical and thalamic neurones during high-voltage rhythmic spike discharge in Long-Evans rats in vivo.

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8.  Enhanced NMDA receptor-dependent thalamic excitation and network oscillations in stargazer mice.

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Journal:  J Neurosci       Date:  2012-08-08       Impact factor: 6.167

9.  The Role of Striatal Feedforward Inhibition in the Maintenance of Absence Seizures.

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Journal:  J Neurosci       Date:  2016-09-14       Impact factor: 6.167

10.  Hardwiring goes soft: long-term modulation of electrical synapses in the mammalian brain.

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Journal:  Cellscience       Date:  2006-01-28
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