Effect of Pharmacological Inactivation of Nucleus Reticularis Tegmenti Pontis on Saccadic Eye Movements in the Monkey

• Published in: Journal of neurophysiology 2006-06, Vol.95 (6), p.3698-3711
• Main Authors: Kaneko, Chris R. S, Fuchs, Albert F
• Format: Article
• Language: English
• Subjects: Animals; Biological Clocks - drug effects; Biological Clocks - physiology; Dose-Response Relationship, Drug; GABA Agonists - administration & dosage; Macaca mulatta; Muscimol - administration & dosage; Nerve Net - drug effects; Nerve Net - physiology; Neural Inhibition - drug effects; Neural Inhibition - physiology; Neural Pathways - drug effects; Neural Pathways - physiology; Neurons - drug effects; Neurons - physiology; Neurotoxins - administration & dosage; Pons - drug effects; Pons - physiology; Reticular Formation - drug effects; Reticular Formation - physiology; Saccades - drug effects; Saccades - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.01292.2005

Department of Physiology and Biophysics and Washington National Regional Primate Research Center, University of Washington, Seattle, Washington Submitted 9 December 2005; accepted in final form 31 January 2006 The superior colliculus (SC) provides signals for the generation of saccades via a direct pathway to the brain stem burst generator (BG). In addition, it sends saccade-related activity to the BG indirectly through the cerebellum via a relay in the nucleus reticularis tegmenti pontis (NRTP). Lesions of the oculomotor vermis, lobules VIc and VII, and inactivation of the caudal fastigial nucleus, the cerebellar output nucleus to which it projects, produce saccade dysmetria but have little effect on saccade peak velocity and duration. We expected similar deficits from inactivation of the NRTP. Instead, injections as small as 80 nl into the NRTP first slowed ipsiversive saccades and then gradually reduced their amplitudes. Postinjection saccades had slower peak velocities and longer durations than preinjection saccades with similar amplitudes. Contraversive saccades retained their normal kinematics. When the gains of ipsiversive saccades to 10° target steps had fallen to their lowest values (0.28 ± 0.19; mean ± SD; n = 10 experiments), the gains of contraversive saccades to 10° target steps had decreased very little (0.82 ± 0.11). Eventually, ipsiversive saccades did not exceed 5°, even to 20° target steps. Moreover, these small remaining saccades apparently were made with considerable difficulty because their latencies increased substantially. When ipsiversive saccade gain was at its lowest, the gain and kinematics of vertical saccades to 10° target steps exhibited inconsistent changes. We argue that our injections did not compromise the direct SC pathway. Therefore these data suggest that the cerebellar saccade pathway does not simply modulate BG activity but is required for horizontal saccades to occur at all. Address for reprint requests and other correspondence: A. F. Fuchs, 1959 NE Pacific St. HSB I421, Washington Regional Primate Research Center, Box 357330, University of Washington, Seattle, WA 98195-7330 (E-mail: fuchs{at}u.washington.edu )