Trigeminal High Frequency Stimulation Produces Short - and Long - Term Modification 4 of Reflex Blink Gain 5 Abbreviated Title : Modifying Reflex Blink Gain

37 Reflex blinks provide a model system for investigating motor learning in normal and 38 pathological states. We investigated whether high frequency stimulation of the supraor39 bital branch of the trigeminal nerve before the R2 blink component (HFS-B) decreases 40 reflex blink gain in alert rats. As with humans (Mao and Evinger 2001), HFS-B signifi41 cantly reduced blink size in the first hour after treatment for rats. Repeated days of HFS42 B treatment produced long-term depression of blink circuits. Blink gain decreased expo43 nentially across days indicating a long-term depression of blink circuits. Additionally, 44 the HFS-B protocol became more effective at depressing blink amplitude across days of 45 treatment. This depression was not habituation because neither longnor short-term 46 blink changes occurred when presenting HFS after the R2. To investigate whether gain 47 modifications produced by HFS-B involved cerebellar networks, we trained rats in a de48 lay eyelid conditioning paradigm using HFS-B as the unconditioned stimulus and a tone 49 as the conditioned stimulus. As HFS-B depresses blink circuits and delay conditioning 50 enhances blink circuit activity, occlusion should occur if they share neural networks. 51 Rats acquiring robust eyelid conditioning did not exhibit decreases in blink gain, whereas 52 rats developing low levels of eyelid conditioning exhibited weak, short-term reductions in 53 blink gain. These results suggested that delay eyelid conditioning and long-term HFS-B 54 utilize some of the same cerebellar circuits. The ability of repeated HFS-B treatment to 55 depress trigeminal blink circuit activity long-term implied that it may be a useful protocol 56 to reduce hyperexcitable blink circuits that underlie diseases like benign essential 57