The sleep spindle rhythm of thalamic origin (7-14 Hz) displays widespread synchronization among thalamic nuclei and over most of the neocortex. 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. Interestingly, the reticularis consists of a population of neurons which are GABAergic and synaptically coupled. These cells, as do thalamic relay cells, exhibit a transient depolarization following release from sustained hyperpolarization. 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 finding that mutual inhibition can in fact synchronize cells, provided that the postsynaptic conductance decays sufficiently slowly. Indeed, postsynaptic receptors of the GABAB subtype mediate inhibition with a large decay time-constant (approximately 200 ms). In contrast, chloride-dependent, GABAA-mediated inhibitory postsynaptic potentials are fast and brief. Both GABAA and GABAB receptor binding sites are present in most thalamic regions, including the reticularis. We suggest that if GABAB receptors exist postsynaptically in the reticularis, they may play a critical role in the rhythmic synchronization among reticular neurons, hence in the thalamocortical system.