The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity

Abstract

Thalamic neurons generate high-frequency bursts of action potentials when a low-threshold (T-type) calcium current, located in soma and dendrites, becomes activated. Computational models were used to investigate the bursting properties of thalamic relay and reticular neurons. These two types of thalamic cells differ fundamentally in their ability to generate bursts following either excitatory or inhibitory events. Bursts generated with excitatory inputs in relay cells required a high degree of convergence from excitatory inputs, whereas moderate excitation drove burst discharges in reticular neurons from hyperpolarized levels. The opposite holds for inhibitory rebound bursts, which are more dif cult to evoke in reticular neurons than in relay cells. The differences between the reticular neurons and thalamocortical neurons were due to different kinetics of the T-current, different electrotonic properties and different distribution patterns of the T-current in the two cell types. These properties enable the cortex to control the sensitivity of the thalamus to inputs and are also important for understanding states such as absence seizures.

A Cav3.2 T-Type Calcium Channel Point Mutation Has Splice-Variant-Specific Effects on Function and Segregates with Seizure Expression in a Polygenic Rat Model of Absence Epilepsy

“…T-type Ca 2ϩ channels underlie a low-threshold spike that plays an important role in the generation of oscillatory thalamocortical rhythms and in the switch between tonic and burst firing patterns (Destexhe and Sejnowski, 2002;Contreras, 2006;Joksovic et al, 2006). Increased Ca v 3.2 expression and increased T-type currents have been detected in the nRT of GAERS and WAG/Rij (Tsakiridou et al, 1995;Talley et al, 2000;Kim et al, 2001;Broicher et al, 2008), suggesting that Ca v 3.2 channels may be a strong candidate for contribution to SWD generation in the thalamocortical network.…”

Encoding of Natural Scene Movies by Tonic and Burst Spikes in the Lateral Geniculate Nucleus

“…It has been shown that the majority of inputs to LGN neurons do not come from the retina (Erisir et al, 1997). During sleep, rhythmic bursting oscillations in the LGN are thought to be controlled by the brainstem (Steriade et al, 1993), whereas bursts observed interspersed with tonic firing in the alert state are thought to be influenced by cortical feedback (Sherman, 2001a;Destexhe and Sejnowski, 2002;Krahe and Gabbiani, 2004). Recently, manipulation of cortical feedback was shown to modulate the proportion of burst and tonic responses in LGN neurons (Wang et al, 2001;Allito et al, 2003).…”

NPY signaling through Y1 receptors modulates thalamic oscillations

“…We cannot however rule out more subtle effects on oscillation parameters exerted by activation of Y 2 (or Y 5 ) receptors, or effects on parameters we did not assay for. Among those might be the initiation or spread of oscillations [6]. Furthermore, these receptors might play different roles in vivo, as circuitry relevant for seizure modulation may not be preserved in the thalamic slice preparation used here.…”

“…NPY signals through a family of six Y receptors (Y 1 -Y 6 , reviewed in 7). In thalamic neurons, Y 1 receptor activation leads to opening of postsynaptically located inwardly rectifying K + (GIRK) channels, which results in a long lasting hyperpolarization.…”