Motor adaptation is an important factor in the recovery of function following motor deficits associated with neural damage due to stroke, injury or aging. Such motor recovery or adaptation, is instructed by an error signal that is calculated by the brain from the mismatch between the desired movement and the actual movement produced. However, the brain circuits that process specific error signal(s) are not understood. The long-term goal of my research is to identify the neural mechanisms that process error signals to optimize sensory-motor behavior. Understanding these mechanisms and the circuitry underlying them will assist in devising rehabilitation therapies for motor deficits. We have approached our goal by using monkey saccadic eye movements, which provide an ideal model because saccades are precise, use only a few muscles, the associated brainstem neural circuit has been well documented and they can be made to undergo motor adaptation by means of well-established behavioral paradigms. Thus far, we know that complex spike firing in the oculomotor vermis (OMV) encodes motor error and that the OMV is required for adaptation of targeting saccades. Complex spikes in the OMV originate in a part of the inferior olive that receives a projection from the superior colliculus (SC). Previously, we have shown that electrical micro-stimulation of the SC, timed to mimic visual error signals, induces saccade adaptation. Thus, the SC appears to be an important part of the error signal pathway. In this study, we propose three projects to test the involvement of the SC in coding an error signal for saccade adaptation. The first project is directed at determining whether the SC is required for adaptation of targeting saccades. We will inactivate the SC reversibly during which time we predict that the monkey will be unable to adapt its saccades when subjected to a behavioral adaptation paradigm. The second project is directed at identifying correlates in SC visual activity with the visual error signal that drives adaptation. We will look for correlations of SC visual activity wit error size (small errors drive adaptation better than large ones) and with adaptation rate, which decreases as adaptation progresses. The third project will determine whether the SC is also used for adaptation of other types of saccade, including memory-guided, delayed, scanning and express. We will electrically stimulate the SC after one of these different types to mimic an error signal and determine whether, as for targeting saccades, this artificial error causes adaptation. I it does, we will test whether the adaptation transfers to the other types. We anticipate that together the results of these three projects will help establish a previously unsuspected role for the SC in saccade adaptation.

Public Health Relevance

Motor adaptation is important in the recovery from deficits subsequent to neural damage such as stroke, injury or aging. A key to inducing motor adaptation is the error signal, i.e., the mismatch between the desired movement and the actual deficit movement, which drives a motor adaptation that reduces the error. In this project, we will investigate the route and characteristics of the neural mechanism of the error signal by using simian saccadic eye movements.

Agency
National Institute of Health (NIH)
Type
Research Project (R01)
Project #
5R01EY023277-02
Application #
8704942
Study Section
(SPC)
Program Officer
Araj, Houmam H
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Washington
Department
Physiology
Type
Schools of Medicine
DUNS #
City
Seattle
State
WA
Country
United States
Zip Code
98195
Kojima, Yoshiko; Robinson, Farrel R; Soetedjo, Robijanto (2014) Cerebellar fastigial nucleus influence on ipsilateral abducens activity during saccades. J Neurophysiol 111:1553-63