Because of its simplicity, blinking is a prominent model system in analysis of adaptation and conditioning with the cerebellum. Nevertheless, data on the role of the cerebellum in modulation of normal reflex blinks are limited. We correlated the discharge of interpositus (IP) neurons with normal trigeminal reflex blinks and blink adaptation in urethane-anesthetized rats. Two groups of IP neurons responded to cornea stimulation. One group, pause neurons, showed a long cessation of their tonic discharge beginning 6 ms before the end of lid closure. The second group, burst neurons, exhibited a transient increase in firing frequency at a constant interval after the cornea stimulus. The cessation of pause neuron activity appeared to contribute to the termination of blinks. The tonic discharge rate increased and the cessation of pause neuron activity was delayed coincident with increased amplitude and duration of reflex blinks produced by blink adaptation. There was a coincident increase in the amplitude and duration of reflex blinks with increased tonic activity and delayed pause in pause neurons treated with the GABA(A) antagonist, gabazine. Burst neurons did not appear to modulate reflex blinks. Burst neuron discharge correlated neither with blink characteristics normally nor with blink adaptation. These findings indicated that pause neurons affect reflex blinks by providing a tonic excitatory input to facial motoneurons during lid closure and then disfacilitating those motoneurons to adjust the termination of lid closure. Burst neurons may play a role in eyelid conditioning.