2011
DOI: 10.1016/j.neuron.2011.02.042
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CaV2.3 Channels Are Critical for Oscillatory Burst Discharges in the Reticular Thalamus and Absence Epilepsy

Abstract: Neurons of the reticular thalamus (RT) display oscillatory burst discharges that are believed to be critical for thalamocortical network oscillations related to absence epilepsy. Ca²+-dependent mechanisms underlie such oscillatory discharges. However, involvement of high-voltage activated (HVA) Ca²+ channels in this process has been discounted. We examined this issue closely using mice deficient for the HVA Ca(v)2.3 channels. In brain slices of Ca(v)2.3⁻/⁻, a hyperpolarizing current injection initiated a low-t… Show more

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Cited by 85 publications
(77 citation statements)
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References 63 publications
(118 reference statements)
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“…Studies in animal models have implicated cortical hyperexcitability and unbalanced excitation/inhibition in the thalamic network, which is consistent with the activity observed in these regions during seizure attacks in humans [110]. Several genetic mouse lines with alterations of nRt excitability represent a good model to test therapeutic interventions for absence epilepsy [9,24,26,27].…”
Section: Sleep Spindles In Pathologymentioning
confidence: 60%
See 1 more Smart Citation
“…Studies in animal models have implicated cortical hyperexcitability and unbalanced excitation/inhibition in the thalamic network, which is consistent with the activity observed in these regions during seizure attacks in humans [110]. Several genetic mouse lines with alterations of nRt excitability represent a good model to test therapeutic interventions for absence epilepsy [9,24,26,27].…”
Section: Sleep Spindles In Pathologymentioning
confidence: 60%
“…Foremost amongst the ionic mechanisms underlying rhythmic nRt bursting are the low-voltage gated T-type Ca 2+ channels (T channels) and the small-conductance Ca 2+ -activated type-2 K + channel (SK2 or Kcnn2 channel). Bursting is additionally shaped by voltage-dependent K + channels [8], R-type channels [9], sarco/endoplasmic reticulum Ca 2+ -ATPases [10], and Ca 2+ -induced Ca 2+ release via ryanodine receptors [11]. However, genetic manipulations of T channels and SK2 channels have proven particularly useful in selectively modifying sleep spindles [12,13].…”
Section: Novel Molecular Aspects Of Spindle Generationmentioning
confidence: 99%
“…The roles, if any, played by other calcium channel subtypes in epileptogenesis await elucidation. Ca V 2.3 (R-type) channels in the thalamus have been implicated in burst firing and potentially proictogenic "plateau potentials" (Randall and Tsien 1997;Metz et al 2005;Zaman et al 2011) with Ca V 2.3 null mice showing an altered susceptibility to absence seizures, as well as resistance to pharmacologically induced limbic seizures, convulsions, and excitotoxic cell death (Weiergraber et al 2006(Weiergraber et al , 2007(Weiergraber et al , 2008, tantalizing data that require further study.…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, low-threshold Ca 2+ currents evoked in Ca V 3.3 −/− cells were invariant against the R-type channel blocker SNX-482 (change by −1.0 ± 2.9%; n = 4, P > 0.05) (Fig. S4) at doses that reduce R currents in nRt slices (20). Around resting membrane potentials, low-threshold Ca 2+ currents thus are carried dominantly by T channels in WT nRt cells and contain two components with different Ni 2+ sensitivity (13 (16).…”
Section: −/−mentioning
confidence: 95%