Krauzlis Lab Projects

Changes in parafoveal tracking caused by inactivation of the

rostral superior colliculus

The rostral superior colliculus (rSC) contributes to the control of fixation, but it is also involved in the generation of smooth pursuit and small saccades. A parsimonious explanation for these seemingly disparate findings is that rSC neurons represent position errors of intended goals on or near the fovea. Consistent with this view, we have recently observed that during parafoveal tracking, rSC neurons exhibit tuning for the position of a foveal goal inferred by peripheral visual stimuli. We have now directly tested the contribution of the rSC to parafoveal tracking by reversible inactivation.

We recorded eye movements in a rhesus macaque that tracked the inferred midpoint (within 5°) between two moving bars (5.4°x0.85°) placed 24° apart at symmetrically opposite locations. The bars were oriented perpendicular to the axis connecting their centers to the screen center, and they moved sinusoidally together along this axis (amp: 4°, freq: 0.7Hz, dur: 3500ms). The axis of motion was chosen in each session to intersect the locations represented by the rSC site visited. In separate blocks, the monkey also tracked a single spot (radius: 0.1°, 1°, 2°) moving along the same axis. We compared the monkey’s tracking movements before (baseline) and after muscimol inactivation (0.5µl, 5µg/µl).

Muscimol inactivation always caused significant increases in the latencies of visually guided saccades to a localized region of space near the center of gaze (affected region). During parafoveal tracking, the monkey’s gaze developed a constant offset (up to 5°) compared to baseline, such that gaze position errors shifted towards the affected region - as if there was an inability to represent or correct for these errors. This offset disappeared, or was significantly smaller, when the monkey tracked a 0.1° spot, and it systematically increased in size with the 1° and 2° spots, respectively - always with a direction shifting gaze position errors towards the affected region.

Our results show that the rSC plays a causal role in parafoveal tracking. These results also indicate that the specification of the tracked goal depends on the population activity of neurons in both rSC. We infer that the size of the observed offset depends on the particular population of rSC neurons normally activated under the different stimulus conditions.

Reference:

Hafed, Z.M., Dill, N., Goffart, L., and Krauzlis, R.J. Changes in parafoveal tracking caused by inactivation of the rostral superior colliculus. Society for Neuroscience Abstract, 2006.



Home: Projects: Changes in parafoveal tracking caused by inactivation of the rostral superior colliculus

	Changes in parafoveal tracking caused by inactivation of the rostral superior colliculus The rostral superior colliculus (rSC) contributes to the control of fixation, but it is also involved in the generation of smooth pursuit and small saccades. A parsimonious explanation for these seemingly disparate findings is that rSC neurons represent position errors of intended goals on or near the fovea. Consistent with this view, we have recently observed that during parafoveal tracking, rSC neurons exhibit tuning for the position of a foveal goal inferred by peripheral visual stimuli. We have now directly tested the contribution of the rSC to parafoveal tracking by reversible inactivation. We recorded eye movements in a rhesus macaque that tracked the inferred midpoint (within 5°) between two moving bars (5.4°x0.85°) placed 24° apart at symmetrically opposite locations. The bars were oriented perpendicular to the axis connecting their centers to the screen center, and they moved sinusoidally together along this axis (amp: 4°, freq: 0.7Hz, dur: 3500ms). The axis of motion was chosen in each session to intersect the locations represented by the rSC site visited. In separate blocks, the monkey also tracked a single spot (radius: 0.1°, 1°, 2°) moving along the same axis. We compared the monkey’s tracking movements before (baseline) and after muscimol inactivation (0.5µl, 5µg/µl). Muscimol inactivation always caused significant increases in the latencies of visually guided saccades to a localized region of space near the center of gaze (affected region). During parafoveal tracking, the monkey’s gaze developed a constant offset (up to 5°) compared to baseline, such that gaze position errors shifted towards the affected region - as if there was an inability to represent or correct for these errors. This offset disappeared, or was significantly smaller, when the monkey tracked a 0.1° spot, and it systematically increased in size with the 1° and 2° spots, respectively - always with a direction shifting gaze position errors towards the affected region. Our results show that the rSC plays a causal role in parafoveal tracking. These results also indicate that the specification of the tracked goal depends on the population activity of neurons in both rSC. We infer that the size of the observed offset depends on the particular population of rSC neurons normally activated under the different stimulus conditions. Reference: Hafed, Z.M., Dill, N., Goffart, L., and Krauzlis, R.J. Changes in parafoveal tracking caused by inactivation of the rostral superior colliculus. Society for Neuroscience Abstract, 2006.
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