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The Journal of Neurophysiology Vol. 83 No. 4 April 2000, pp. 2285-2299
Copyright ©2000 by the American Physiological Society
Department of Neurology, The University of Connecticut Health Center, Farmington, Connecticut 06030
Waitzman, David M.,
Valentine L. Silakov,
Stacy DePalma-Bowles, and
Amanda S. Ayers.
Effects of Reversible Inactivation of the Primate Mesencephalic
Reticular Formation. II. Hypometric Vertical Saccades. J. Neurophysiol. 83: 2285-2299, 2000. Electrical microstimulation and single-unit recording have suggested
that a group of long-lead burst neurons (LLBNs) in the mesencephalic
reticular formation (MRF) just lateral to the interstitial nucleus of
Cajal (INC) (the peri-INC MRF, piMRF) may play a role in the generation
of vertical rapid eye movements. Inactivation of this region with
muscimol (a GABAA agonist) rapidly produced vertical
saccade hypometria (6 injections). In three of six injections, there
was a marked reduction in the velocity of vertical saccades out of
proportion to saccade amplitude (i.e., saccades fell below the main
sequence). This was associated with a moderate increase in saccade
duration. Inadvertent inactivation of the INC could not account for
these observations because vertical, postsaccadic drift was not
observed. Similarly, pure downward saccade hypometria, the hallmark of
rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) inactivation, was always preceded by loss of upward saccades in our experiments. We also found a downward and ipsiversive displacement of initial eye position and evidence of a
contraversive head tilt following piMRF injections. Saccade latency was
shorter after two of six injections. Simulation of a local feedback
model provided three possible explanations for vertical saccade
hypometria: 1) a shift in the input to the model to
request smaller saccades, 2) a reduction of LLBN input
to the vertical saccade medium lead burst neurons (MLBNs), or
3) an increase in the gain of the feedback pathway.
However, when the second hypothesis was coupled to a shortened duration
of the saccade trigger (i.e., the discharge of the omnipause neurons),
the physiological observations of piMRF inactivation could be
replicated. This suggested that muscimol had targeted structures that
provided both long-lead burst activity to the MLBNs in the riMLF and
were critical for reactivation of the omnipause neurons. Evidence of
markedly reduced vertical saccade amplitude, curved saccade
trajectories, increased saccade duration, and saccades that fall below
the amplitude/velocity main sequence in these monkeys closely parallels
the oculomotor findings of patients with progressive supranuclear palsy (PSP).
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