P153 Cerebellar-M1 connectivity (CBI): One or two different networks?

Introduction Recently it has been argued that two distinct interneuron networks in the primary motor cortex (M1) contribute distinctly to two varieties of physiological plasticity and motor behaviors (Hamada et al., 2014). Although one of the interneuron groups is thought to be dependent on cerebellar (CB) activity, direct physiological distinction regarding CB-M1 interactions (CBI) to these subpopulations remains poorly understood. Objectives This study assessed whether M1 coil orientation, thought to test different neuronal populations, affects CBI in the context of two motor behaviors that weight differently cerebellar vs. M1 contributions. Methods In experiment 1 (n = 10), we tested the effect of coil orientation (posterior–anterior, PA; anterior–posterior, AP) and inter-stimulus intervals (ISI: 3, 5 and 7 ms) on CBI; assessed with a conditioned TMS pulse over the cerebellum prior to TMS over the contralateral M1. In experiment 2 (n = 10), we tested how learning two distinct motor learning tasks (weighting sensorimotor calibration vs. a sequence task) affected AP- vs. PA-CBI measured at their preferential ISI. Results ANOVA-RM revealed a significant CBI effect for ISI (F(2,36) = 17.807; p < 0.01) and COIL ORIENTATION*ISI interaction (F(2,36) = 8.067; p = 0.01). Specifically, PA-CBI was prominent at 5 ms ISI (p = 0.02) and AP-CBI at 7 ms ISI (p = 0.01). To determine how learning affects AP- vs. PA-CBI at their preferential ISI, we compared CBI before, during and after training. ANOVA-RM revealed a significant effect of CBI for MOTOR TASK*TIME*ORIENTATION interaction (F(4,42) = 2.800; p = 0.04). When learning a sensorimotor calibration, PA-CBI changed only early during learning (p = 0.02), whereas AP-CBI changed only late (p = 0.01). Additionally, during sequence learning, PA-CBI also changed only early (p = 0.01), whereas AP-CBI was not modulated. Conclusion These findings indicate that CB-M1 interactions are different for the two M1 neural networks. This could be the result of either two independent CB-M1 pathways or distinct processing of cerebellar inputs within M1.