, 2004). With such asymmetry in the spatial pattern of activity across the SC, the center of mass of foveal SC activity may shift sufficiently away
from bilateral balance that it exceeds the threshold for triggering a microsaccade (Hafed et al., 2009). Because these microsaccades directed towards the attended location shift the representation of the entire visual field, including the fixation stimulus, they could precipitate subsequent imbalances in the opposite direction, Sotrastaurin mw promoting a sequence of microsaccades towards and away from the attended location. When the SC is inactivated, the asymmetry caused by attentional allocation is eliminated or even reversed (Lovejoy & Krauzlis, 2010), explaining the directional redistribution of microsaccades that we observed. Thus, unlike inactivation of the rostral (or foveal) SC, which reduces microsaccade rate, the results from our current study demonstrate another way in which SC activity contributes to microsaccade generation – by influencing the probability of triggering microsaccades, without necessarily affecting the motor generation selleck screening library of these movements. For early cue-induced influences on microsaccades (Figs 6-9), cue-induced visual bursts in the peripheral SC can acetylcholine also transiently
modify activity patterns in the above-mentioned model, explaining why microsaccades are modulated during exogenously driven covert attention shifts (as in the initial microsaccade biases in Figs 8 and 9). Specifically, in addition to the nominal goal representation of the fixated target in the above model,
when a peripheral stimulus appears on the display, a strong visual burst is induced in the SC at the anatomical site in this structure representing the stimulus location. Moreover, the strength of this burst may be modulated by attention, among other factors (Boehnke & Munoz, 2008). Thus, one possible mechanism for how abruptly appearing attentional cues can give rise to an initial bias in microsaccade directions is, again, through biasing the population average activity in the entire SC map – this time by introducing a transient increase in activity at the SC site corresponding to the peripheral cue location (and other possible transient changes in activity in other locations in the SC retinotopic map). Thus, the model of Hafed et al. (2008, 2009), along with the transient changes in SC neurons that are expected to occur across the map as a result of cue and foil onset, can explain the patterns of results that we obtained both with and without inactivation.