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This Article Full Text Full Text (PDF) All Versions of this Article: 100/4/1949    most recent 90526.2008v3 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Soetedjo, R. Articles by Fuchs, A. F. PubMed PubMed Citation Articles by Soetedjo, R. Articles by Fuchs, A. F.

Complex Spike Activity in the Oculomotor Vermis of the Cerebellum: A Vectorial Error Signal for Saccade Motor Learning?

Departments of Physiology and Biophysics and Washington National Primate Research Center, University of Washington, Seattle, Washington

Submitted 1 May 2008; accepted in final form 24 June 2008

Brain stem signals that generate saccadic eye movements originate in the superior colliculus. They reach the pontine burst generator for horizontal saccades via short-latency pathways and a longer pathway through the oculomotor vermis (OMV) of the cerebellum. Lesion studies implicate the OMV in the adaptation of saccade amplitude that occurs when saccades become inaccurate because of extraocular muscle weakness or behavioral manipulations. We studied the nature of the possible error signal that might drive adaptation by examining the complex spike (CS) activity of vermis Purkinje (P-) cells in monkeys. We produced a saccade error by displacing the target as a saccade was made toward it; a corrective saccade 200 ms later eliminated the resulting error. In most P-cells, the probability of CS firing changed, but only in the error interval between the primary and corrective saccade. For most P-cells, CSs occurred in a tight cluster 100 ms after error onset. The probability of CS occurrence depended on both error direction and size. Across our sample, all error directions were represented; most had a horizontal component. In more than one half of our P-cells, the probability of CS occurrence was greatest for error sizes <5° and less for larger errors. In the remaining cells, there was a uniform increased probability of CS occurrence for all errors 7–9°. CS responses disappeared when the target was extinguished during a saccade. We discuss the properties of this putative CS error signal in the context of the characteristics of saccade adaptation produced by the target displacement paradigm.