A pharmacological distinction between the long and short latency pathways of the human blink reflex revealed with tobacco.

In three, normal, human subjects, tobacco smoking was used as a pharmacological probe to modify differentially the direct and indirect pathways underlying the blink reflex. The latency of the indirect R2 component of the orbicularis oculis electromyogram evoked by electrical stimulation of the trigeminal supraorbital nerve transiently increased 20-80% after smoking, while the latency of the shorter latency, direct R1 component remained constant. The magnitude of both components of the blink reflex transiently decreased. The data demonstrate that tobacco smoking can differentially alter the long and short latency components of the blink reflex, and suggest that these effects result from modifications of central pathways sensitive to nicotine.