Abstract
It has been shown that the nucleus of the optic tract (NOT) is an important visuomotor relay between the retina and preoculomotor structures, and is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits, and rats. The details between the NOT and the vestibular nucleus in the brain stem concerning the morphology of fibers-of-passage and axon terminals have been disclosed in cats and monkeys. One is that they project to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs, the posterior commissure was cut in the present experient. Three fuscata monkeys (M17, M19, M22) were used. A magnetic search coil was sutured to the right eye to record eye position. Several bolts were embedded and secured with dental acrylic cement to fasten the animal's head during experiments. The animal was mounted on a turn table covered by an OKN screen, onto which OKN stripes were projected from above. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and bilateral eye viewing. OKN was recorded in response to counter clockwise (CCW) and clockwise (CW) stimulation at stimulus velocities of 30°/s, 60°/s, and 90°/s. After the control experiment was completed, the posterior commissure was transected by an operator knife. After follow-up studies were completed, an anterograde tracer was injected in the left NOT to ascertain the complete block between NOTs. Rapid rise (RR) and steady state (SS) of slow-phase OKN velocity and time-constants (TC) of optokinetic afternystagmus (OKAN) were measured. In three aniamis, OKN gains elicited with monocular viewing were approximately equal to the those of binocularly-evoked OKN before and after surgery. In the three monkeys, the commissurectomy decreased RR and SS to both sides during the three weeks immediately after surgery. In M22, TC showed the tendency to decrease by only 30°/s and 60°/s after surgery. There were no significant differences in TCs of other experiments.In conclusion, gain reduction in RR and SS can be explained by decrease of inhibiting the resting rate in NOT, which is conducted via commissural fibers. This was caused by interruption due to a middle-line lesions. Furthermore, interrupting the commissural fibers has nothing to do with the velocity storage mechanism.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
