SPINDLE RHYTHMICITY IN THE RETICULARIS-THALAMI NUCLEUS - SYNCHRONIZATION AMONG MUTUALLY INHIBITORY NEURONS

The sleep spindle rhythm of thalamic origin (7-14 Hz) displays widespread synchronization among thalamic nuclei and over most of the neocortex.1 The mechanisms which mediate such global synchrony are not yet well understood. Here, we theoretically address the hypothesis of Steriade and colleagues that the reticularis thalami nucleus may be considered as a genuine pacemaker for thalamocortical spindles.29-31 Interestingly, the reticularis consists of a population of neurons15,25 which are GABAergic and synaptically Coupled.9,21,23,35 These cells, as do thalamic relay cells,10,17-18 exhibit a transient depolarization following release from sustained hyperpolarization.2,19,22,28 This postinhibitory rebound property is due to a T-type calcium ionic current which is inactivated at rest but de-inactivated by hyperpolarization. Theoretically, rebound-capable cells coupled by inhibition can generate rhythmic activity, although such oscillations are usually alternating (out-of-phase), rather than synchronous (in-phase).'' Here, we develop and apply to Steriade's pacemaker hypothesis our earlier finding34 that mutual inhibition can in fact synchronize cells, provided that the postsynaptic conductance decays sufficiently slowly. Indeed, postsynaptic receptors of the GABA(B) subtype mediate inhibition with a large decay time-constant (congruent-to 200 ms).13 In contrast, chloride-dependent, GABA(A)-mediated inhibitory postsynaptic potentials are fast and brief. Both GABA(A) and GABA(B) receptor binding sites are present in most thalamic regions, including the reticularis.4,6 We suggest that if GABA(B) receptors exist postsynaptically in the reticularis, they may play a critical role in the rhythmic synchronization among reticular neurons, hence in the thalamocortical system.