Contrary to this hypothesis, we found that the firing rate excursion was significantly larger in the Fast condition than the Accurate condition for the vast majority of neurons, irrespective of neuron type (Figure S4). The variety and direction of neural adjustments we observed during SAT does not correspond intuitively to the account of SAT provided by stochastic accumulator models. Reconciliation begins with the recognition that the brainstem circuitry responsible for saccade production places constraints on the form that SC and FEF movement activity can this website take. Stochastic accumulator models overlook these considerations because the terminal motor stage lies outside the model.
This, along with a
stimulus encoding stage, is captured simply by a residual time parameter. However, much is known about the anatomy, physiology, and chronometry of these afferent and efferent stages for saccades during visual search. The following considerations demonstrate that brainstem neurons receiving movement neuron output reach a fixed level of activity across all SAT conditions when saccades are initiated. The burst neurons in the brainstem responsible for producing contraction of the extraocular muscles are gated by omnipause neurons (OPNs; Büttner-Ennever et al., 1988; Scudder et al., Buparlisib purchase 2002; Kanda et al., 2007; Shinoda et al., 2008; Van Horn et al., 2010; Figure S5A). In their default state, OPNs prevent saccade generation through tonic inhibition of burst neurons; saccades are initiated precisely when this inhibition is released. Movement cells in FEF, SC, and elsewhere initiate saccades through direct, and ultimately inhibitory, projections to
OPN (Raybourn and Keller, 1977; Huerta et al., 1986; Stanton et al., 1988; Segraves, 1992). Crucially, saccade velocity scales with the magnitude of OPN hyperpolarization (Yoshida et al., 1999). The invariance of saccade velocity across hundreds of milliseconds of RT variation across SAT conditions (Figure 1) entails Ergoloid that the level of OPN hyperpolarization must be invariant across SAT conditions. How can the level of OPN hyperpolarization be invariant across SAT conditions if presaccadic movement neuron activity varies across SAT conditions? An answer is offered through the observation that neurons are leaky integrators. Consequently, the OPN response to FEF movement activity is a function of both its magnitude and rate of increase over time. In our data, the influence of FEF movement neurons on OPN is lower and slower in the Accurate condition and higher but briefer in the Fast condition. We reasoned that we could approximate the net inhibition onto OPN by submitting the movement neuron activity to leaky integration. For each movement neuron and each trial, activity was integrated with leak from search array presentation until saccade initiation (Experimental Procedures).