Role of the thalamic reticular nucleus in the generation of rhythmic thalamo-cortical activities subserving spike and waves

Avanzini, Giulio; Curtis, Marco de; Marescaux, C.; Panzica, Ferruccio; Spreafico, Roberto; Vergnes, M.

doi:10.1007/978-3-7091-9206-1_6

Cited by 66 publications

(66 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been argued that thalamic T-type channels and hence the GABA B receptors that deinactivate them are critical for SWD (Crunelli and Leresche, 1991;Avanzini et al, 1992Avanzini et al, , 1993Hosford et al, 1992;Liu et al, 1992;Marescaux et al, 1992;von Krosigk et al, 1993;Bal et al, 1995;Tsakiridou et al, 1995;Danober et al, 1998;Kim et al, 2001). When VM neurons are in the bursting mode, their firing rate increases abruptly at threshold crossing (Sherman, 2006).…”

Section: Consistency With Previous Experimental Resultsmentioning

confidence: 99%

“…They can be recorded in electroencephalograms (EEGs) as spike-andwave discharges (SWDs) (Gibbs et al, 1935). In animal models of absence epilepsy, SWDs are abolished by lesions or inactivations of the cortex or the thalamus (Avoli and Gloor, 1982;Vergnes and Marescaux, 1992;Meeren et al, 2005Meeren et al, , 2009Polack et al, 2009). These experimental results led to the thalamocortical the-ory that the interactions between the thalamus and the cortex generate absence seizures (Prince and Farrell, 1969;Destexhe, 1998Destexhe, , 2007Avoli, 2012).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2016

View full text Add to dashboard Cite

Absence seizures are characterized by brief interruptions of conscious experience accompanied by oscillations of activity synchronized across many brain areas. Although the dynamics of the thalamocortical circuits are traditionally thought to underlie absence seizures, converging experimental evidence supports the key involvement of the basal ganglia (BG). In this theoretical work, we argue that the BG are essential for the maintenance of absence seizures. To this end, we combine analytical calculations with numerical simulations to investigate a computational model of the BG-thalamo-cortical network. We demonstrate that abnormally strong striatal feedforward inhibition can promote synchronous oscillatory activity that persists in the network over several tens of seconds as observed during seizures. We show that these maintained oscillations result from an interplay between the negative feedback through the corticosubthalamo-nigral pathway and the striatal feedforward inhibition. The negative feedback promotes epileptic oscillations whereas the striatal feedforward inhibition suppresses the positive feedback provided by the cortico-striato-nigral pathway. Our theory is consistent with experimental evidence regarding the influence of BG on seizures (e.g., with the fact that a pharmacological blockade of the subthalamo-nigral pathway suppresses seizures). It also accounts for the observed strong suppression of the striatal output during seizures. Our theory predicts that well-timed transient excitatory inputs to the cortex advance the termination of absence seizures. In contrast with the thalamocortical theory, it also predicts that reducing the synaptic transmission along the cortico-subthalamo-nigral pathway while keeping constant the average firing rate of substantia nigra pars reticulata reduces the incidence of seizures.

show abstract

Section: Consistency With Previous Experimental Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Nimodipine may block sodium and glutamate as well as calcium-dependent potassium and chloride channels in a dose range that modulates epilepsy (Jones and Heinemann, 1987;Aicardi et al, 1990). Avanzini et al (1992) suggested that blockade of calcium channels is the mechanism underlying inhibition of spike-wave discharges. They showed that cadmium, which blocks both the calcium and the calcium-dependent potassium channels, suppressed repetitive burst discharges in vitro and decreased the number of spike-wave discharges in vivo.…”

Section: Resultsmentioning

confidence: 99%

Role of L‐Type Calcium Channel Modulation in Nonconvulsive Epilepsy in Rats

1995

View full text Add to dashboard Cite

Summary: Old male Wistar rats spontaneously showing hundreds of spike-wave discharges daily were used to investigate the role of calcium ions in nonconvulsive epilepsy. The effects of the L-type calcium channel blocker nimodipine and the L-type channel opener BAY K 8644 on number and duration of these spike-wave discharges were investigated. In rats aged 84-94 weeks standard EEG electrodes were chronically implanted; animals were allowed to recover for 10 days. After a baseline registration, nimodipine 2.2, 8.8, and 35.2 mgkg or BAY K 8644 in dosages of 0.12, 0.47, and 1.88 mg/kg was administered. A control group received the solvent. EEG recordings were made to evaluate drug effects. The highest dose of nimodipine increased the number of spikewave discharges, whereas BAY K 8644 reduced the number of spike-wave discharges dose dependently. The high-

show abstract

“…Thalamic neurons have the ability to shift between an oscillatory and burst firing mode (23) where this shift is important in the regulation of external stimuli. Oscillatory neuronal behavior of the circuit is driven by the reticular thalamic nucleus that is situated between the thalamus and the cortex to influence the flow of information (24). The reticular thalamic nucleus comprises mainly of GABA-containing neurons projecting to the thalamic relay nuclei (25).…”

Section: +mentioning

confidence: 99%

The Effects of Ethosuximide on Amino Acids in Genetic Absence Epilepsy Rat Model

et al. 2006

View full text Add to dashboard Cite

Abstract. Genetic absence epilepsy rats from Strasbourg (GAERS), a selectively inbred strain of Wistar rats, has been validated as an experimental model for human absence epilepsy. In this model, systemic administration of ethosuximide (ETX) was shown to reduce the spike and wave discharges (SWD). In this study, γ-aminobutyric acid (GABA) and L-glutamic acid levels in response to ETX injections (i.p., 100 mg / kg) were measured in the microdialysis samples collected from the ventrolateral thalamus (VLT) and the primary motor cortex (M1) area of Wistar rats and GAERS by using HPLC with fluorescent detection. Throughout the microdialysis procedure, continuous EEG recording was performed where ETX was shown to suppress the SWD activity. We demonstrated increased basal GABA levels in the M1 and VLT of GAERS, and ETX treatment did not produce any effect on higher GABA levels in the VLT, but suppressed the increased GABA levels significantly in the M1 of GAERS. All these findings denote the importance of corticothalamic circuitry and the role of increased GABA tonus in primary motor cortex and thalamus of GAERS. The primary motor cortex also seems to be involved in the SWD activity and ETX exerts, at least partially, its neurotransmitter effects through it.

show abstract

Role of the thalamic reticular nucleus in the generation of rhythmic thalamo-cortical activities subserving spike and waves

Cited by 66 publications

References 22 publications

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

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

Role of L‐Type Calcium Channel Modulation in Nonconvulsive Epilepsy in Rats

The Effects of Ethosuximide on Amino Acids in Genetic Absence Epilepsy Rat Model

Contact Info

Product

Resources

About