During relaxed wakefulness, the human brain exhibits pronounced rhythmic electrical activity in the α frequency band (8-13 Hz). This activity consists of 3 main components: the classic occipital α rhythm, the Rolandic μ rhythm, and the so-called third rhythm. In recent years, the long-held belief that α rhythms are strongly influenced by the thalamus has been confirmed in several animal models and, in humans, is well supported by numerous noninvasive imaging studies. Of specific importance is the emergence of 2 key cellular thalamic mechanisms, which come together to generate locally synchronized α activity. First, a novel form of rhythmic burst firing, termed high-threshold (HT) bursting, which occurs in a specialized subset of thalamocortical (TC) neurons, and second, the interconnection of this subset via gap junctions (GJs). Because repetitive HT bursting in TC neurons occurs in the range of 2 to13 Hz, with the precise frequency increasing with increasing depolarization, the same cellular components that underlie thalamic α rhythms can also lead to θ (2-7 Hz) rhythms when the TC neuron population is less depolarized. As such, this scenario can explain both the deceleration of α rhythms that takes place during early sleep and the chronic slowing that characterizes a host of neurological and psychiatric disorders.