The proposed research will continue our studies of pontine and medullary brainstem structures that are part of, or modulate, pathways to ocular motoneurons. Two different project lines will be followed, each of which will employ alert behaving monkeys. Eye position will be accurately measured by an electromagnetic technique and the animal will be trained to track a small moving light spot while subjected to whole body oscillations and full-field movements of the visual world. In one project, the behavior of the saccadic system will be studied by three different approaches designed to distinguish between the traditional Robinson burst generator model and a modified version developed in our lab (Scudder, 1988). First, unit activity will be recorded in the rostral pons to describe both possible visual sensitivity and the motor sensitivity of long lead burst neurons (LLBns): Second, stimulating electrodes placed in various sites of the superior colliculus will be used to activate LLBNs. Second, stimulating electrodes placed in various sites of the superior colliculus will be used to activate LLBNs to ascertain the topographic weighting of the collicular input to the burst generator. Third, simultaneous recordings from collicular burst neurons and LLBNs or LLbns and other elements of the burst generator (e.g., EBNs) will be used to perform cross-correlation analyses to reveal neuronal connections. In the other project, the role of the vestibular nuclei and its apparentally the nucleus prepositus (NPH) in the generation of eye and head movements will be studied in 6 separate projects. First, the visual signals reaching the vestibular nuclei and NPH will be investigated in trained animals to allow the behavioral identification of the various neuronal types. Second, the connections of vestibular nucleus and NPH neurons to the abducens nuclei will be revealed by spike- triggered averages of lateral rectus muscle EMG activity triggered by the action potentials of candidate premotor cells. Third, the degree of canal-canal convergence in these medullary neurons will be investigated by our new multi-axis turntable. Fourth, inputs to subgroups of neurons in the vestibular nuclei and NPH will be identified by physiologically- guided HRP injections. Fifth, lesions of the NPH will be made to confirm its role as the legendary neural integrator. Sixth, the neurons sending descending commands to cervical motoneurons will be identified by antidromic activation and their discharge patterns determined during passive and active head rotations. Studies such as these that demonstrate the pathways and neural structure involved in different types of eye movements make it possible to devise clinical tests to diagnose the site o lesions or strokes that cause specific eye movement disorders in human patients (See Leigh & Zee, The Neurology of Eye Movements: F.A. Davis Co., Philadelphia 1983).
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