While the baseline EMG activity can explain a portion of the response differential on pro- vs. anti-saccade in this timeframe (e.g. the last three stimulation points), our data show that a larger degree of interaction persists on anti-saccade vs. pro-saccade trials (histograms in Figs 5 and 6). How then can we reconcile larger evoked neck muscle responses on anti-saccade trials with the accompanying disruptions of anti-saccade PF-02341066 research buy performance? We begin

by first considering the latency of the neck muscle response evoked by ICMS-SEF. As shown in Fig. 4A, the latency of the evoked neck muscle response is very short, beginning 25–30 ms after stimulation onset and peaking after the stimulation train. We have previously quantified PI3K inhibitor neck muscle response latencies to ICMS-SEF using a variety of methods to be in the range of 30 ms, leading any evoked saccades by ~40–70 ms on average (Chapman et al., 2012). The large difference between the onset latencies of neck muscle responses vs. saccades permits the use of short-duration stimulation as a probe of the excitability of the oculomotor system (Corneil et al., 2007). The short latency of the evoked neck muscle response implicates a largely feedforward mechanism from the frontal cortex, through the

oculomotor brainstem, and from there to spinal cord and motor periphery. The SEF is connected to a number of oculomotor areas within the brainstem, including the intermediate layers of the SC and other oculomotor structures in the pontomedullary reticular formation; either of these could serve as intermediary relays between the Amobarbital SEF and spinal cord [see Chapman et al. (2012) for more

detailed considerations]. It is also possible that the SEF’s influence over neck muscle recruitment is mediated through the FEF, as neck muscle response latencies from this structure are ~5–10 ms shorter than from the SEF (Elsley et al., 2007). Regardless of the precise cortical route, the greater responsiveness of the cephalo- vs. oculomotor circuits is consistent with a series of results in humans and monkeys showing correlates of imposed or adopted subthreshold oculomotor plans in the motor periphery at the neck (Corneil et al., 2004, 2008; Rezvani & Corneil, 2008; Goonetilleke et al., 2010, 2011). We (Corneil, 2011) and others (Galiana & Guitton, 1992; Pélisson et al., 2001; Gandhi & Sparks, 2007) have emphasized the potential role of the omni-pause neurons in the brainstem, which appear to selectively inhibit premotor oculomotor circuits for saccadic gaze shifts without imparting a similar level of influence on cephalomotor commands. Our results also have implications for a potential role of the SEF in eye–head coordination. A central question in motor coordination is how the brain selects a particular pattern of multisegmental coordination from a limitless space of solutions that could all achieve a desired goal (Bernstein, 1967).