Output from the cerebellum is critical to making accurate voluntary rapid eye movements, called saccades. Accurate saccades are essential to our clearly seeing the world around us because the high-resolution part of the eye, the fovea, is very small. To see clearly we must aim the fovea quickly and accurately at the things we want to see. Patients with damage to the eye movement part of the cerebellum cannot make accurate saccades and have a very difficult time seeing the world around them. ? ? The cerebellar output influencing the horizontal component of saccades consists of action potential bursts from neurons inside the cerebellum, the caudal fastigial nucleus (CFN). CFN cells on one side of the cerebellum exhibit action potential bursts early in saccades away from that side (contraversive saccades). These early bursts help accelerate contraversive saccades. CFN cells also burst later for saccades toward the side they are on (ipsiversive saccades). These bursts help decelerate ipsiversive saccades. ? ? The later decelerating, burst for ipsiversive saccades influences saccades much more than the early, accelerating burst does. It is also largely responsible for making saccades accurate. No signal going into the cerebellum resembles these late decelerating bursts so the cerebellum almost certainly produces them by changing the signals that it receives. ? ? We propose that the cerebellum generates late, decelerating, CFN bursts by delaying saccade-related signals that come from outside the cerebellum. It delays these signals by conducting them through the eye movement part of the cerebellum in axons called parallel fibers (p-fibers). If this is true, then interrupting p-fibers in the eye movement part of the cerebellum will abolish the late burst in CFN neurons. Saccades will not decelerate enough so they will overshoot their targets. The work proposed here will conclusively test this hypothesis by measuring saccades after we cut the p-fibers in the eye movement part of the cerebellum. ? ?

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Small Research Grants (R03)
Project #
1R03EY014590-01
Application #
6598213
Study Section
Special Emphasis Panel (ZEY1-VSN (01))
Program Officer
Hunter, Chyren
Project Start
2003-04-04
Project End
2006-03-31
Budget Start
2003-04-04
Budget End
2004-03-31
Support Year
1
Fiscal Year
2003
Total Cost
$160,000
Indirect Cost
Name
University of Washington
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Buzunov, Elena; Ojemann, Jeffrey G; Robinson, Farrel R (2010) Rhesus macaque as an animal model for posterior fossa syndrome following tumor resection. Pediatr Neurosurg 46:120-6
Crook, J D; Hendrickson, A; Erickson, A et al. (2007) Purkinje cell axon collaterals terminate on Cat-301+ neurons in Macaca monkey cerebellum. Neuroscience 149:834-44
Crook, J; Hendrickson, A; Robinson, F R (2006) Co-localization of glycine and gaba immunoreactivity in interneurons in Macaca monkey cerebellar cortex. Neuroscience 141:1951-9