Essentially, the evolution of a neck muscle response in the absen

Essentially, the evolution of a neck muscle response in the absence of a saccade arises from the selective inhibition of omni-pause neurons on saccadic, but not cephalomotor, elements (see above). An alternative mechanism is required to explain the disruptive effects of ICMS-SEF on bilateral anti-saccade ERK inhibitor behavior. We surmise that such behavioral effects are manifest via a disruptive effect of ICMS-SEF on oculomotor activity that largely plays out

after the cessation of stimulation. In Fig. 7, we illustrate this as a decrease in accumulating SEF and SC activity away from saccade threshold (as suggested by Kunimatsu & Tanaka, 2012), with greater delays being present on anti- vs. pro-saccade Pexidartinib concentration trials given the larger role for the SEF in this behavior. In contrast to the feedforward and lateralized influence on neck muscle activity, we suggest that such disruption arises from feedback pathways, perhaps through the thalamus as noted above. Although data from the SEF is lacking, the FEF undergoes a large and prolonged period of hyperpolarization after electrical stimulation (Seidemann et al., 2002) that was suggested to involve the other, non-stimulated FEF. Whether this is also true of the SEF remains

to be determined, but given the results of Seidemann and colleagues, a multiphasic response to ICMS within the SEF that consists of an initial excitation followed by a prolonged period of inhibitions seems plausible. One key prediction of our speculative mechanism is that such inhibition is itself state-dependent, being greater or perhaps more

long-lasting on anti- vs. pro-saccade trials. Disruption of the habitual evolution of SEF activity on anti-saccades would also increase the propensity of anti-saccade errors (not illustrated). The diversity of effects evoked by ICMS-SEF provides a novel perspective on the effects of stimulation of a high-level area such as the SEF on behavior. ICMS-SEF can disrupt some aspects of oculomotor behavior while facilitating others, and future studies will need to determine whether the co-existence of disruptive tuclazepam and facilitative effects is unique to the SEF and to ICMS. In light of our results, functional interpretations based on state-dependent results should consider not only the direction of such influences (i.e. whether stimulation ostensibly disrupts or facilitates behavior), but also how such state-dependent results are assessed. To illustrate this, had we only looked at anti-saccade behavior, a plausible interpretation would be that ICMS selectively disrupts SEF processing for anti-saccades. Yet had we only looked at neck muscle recruitment, a plausible interpretation would have been that ICMS-SEF facilitates contralateral orienting for anti-saccades.

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