The hypothesis that the functional role of the sleep spindle is to preserve sleep by inhibiting sensory input (Yamadori 1971) was examined. Series of 44 dB, 10 msec, 1000 c/sec 'clicks' were presented to 12 subjects at a 30-sec ISI during stage 2 sleep either during spindle bursts (i.e. spindle-synchronous clicks) or during interburst periods (i.e. spindle-asynchronous clicks). Contrary to the spindle inhibitory hypothesis, cortical EEG and cardiovascular responses showed no evidence of spindle 'suppression'. Evoked K-complexes were potentiated by the spindle-synchronous stimulation. A second study with 7 subjects replicated this result and extended the finding to include stage 3--4 sleep. It was suggested that the potentiation of evoked K-complexes was due to phasic reductions in inhibitory action during sleep spindles resulting in increased transmission of sensory events or, perhaps, an increase in the lability of certain EEG response systems.