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Characteristics of Saccadic Gain Adaptation in Rhesus Macaques

Characteristics of Saccadic Gain Adaptation in Rhesus Macaques Abstract Straube, Andreas, Albert F. Fuchs, Susan Usher, and Farrel R. Robinson. Characteristics of saccadic gain adaptation in rhesus macaques. J. Neurophysiol. 77: 874–895, 1997. We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15° and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate. Footnotes Address for reprint requests: A. F. Fuchs, Regional Primate Research Center, Box 357330, University of Washington, Seattle, WA 98195-7330. Present address of A. Straube: Neurological Clinic, Ludwig-Maximilians University, Munich, Germany. Copyright © 1997 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurophysiology The American Physiological Society

Characteristics of Saccadic Gain Adaptation in Rhesus Macaques

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The American Physiological Society
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Copyright © 2011 the American Physiological Society
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0022-3077
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1522-1598
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Abstract

Abstract Straube, Andreas, Albert F. Fuchs, Susan Usher, and Farrel R. Robinson. Characteristics of saccadic gain adaptation in rhesus macaques. J. Neurophysiol. 77: 874–895, 1997. We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15° and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate. Footnotes Address for reprint requests: A. F. Fuchs, Regional Primate Research Center, Box 357330, University of Washington, Seattle, WA 98195-7330. Present address of A. Straube: Neurological Clinic, Ludwig-Maximilians University, Munich, Germany. Copyright © 1997 the American Physiological Society

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Journal of Neurophysiology – The American Physiological Society

Published: Feb 1, 1997

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