Trigeminal reflex blinks evoked near the onset of a saccade cause profound
spatial-temporal perturbations of the saccade that are typically compensate
d in mid-flight. This paper investigates the influence of reflex blinks on
the discharge properties of saccade-related burst neurons (SRBNs) in interm
ediate and deep layers of the monkey superior colliculus (SC). Twenty-nine
SRBNs, recorded in three monkeys, were tested in the blink-perturbation par
adigm. We report that the air puff stimuli, used to elicit blinks, resulted
in a short-latency (similar to 10 ms) transient suppression of saccade-rel
ated SRBN activity. Shortly after this suppression (within 10-30 ms), all n
eurons resumed their activity, and their burst discharge then continued unt
il the perturbed saccade ended near the extinguished target. This was found
regardless whether the compensatory movement was into the cell's movement
field or not. In the limited number of trials where no compensation occurre
d, the neurons typically stopped firing well before the end of the eye move
ment. Several aspects of the saccade-related activity could be further quan
tified for 25 SRBNs. It appeared that 1) the increase in duration of the hi
gh-frequency burst was well correlated with the (two- to threefold) increas
e in duration of the perturbed movement. 2) The number of spikes in the bur
st for control and perturbed saccades was quite similar. On average, the nu
mber of spikes increased only 14%, whereas the mean firing rate in the burs
t decreased by 52%. 3) An identical number of spikes were obtained between
control and perturbed responses when burst and postsaccadic activity were b
oth included in the spike count. 4) The decrease of the mean firing rate in
the burst was well correlated with the decrease in the velocity of perturb
ed saccades. 5) Monotonic relations between instantaneous firing rate and d
ynamic motor error were obtained for control responses but not for perturbe
d responses. And 6) the high-frequency burst of SRBNs with short-lead and l
ong-lead presaccadic activity (also referred to as burst and buildup neuron
s, respectively) showed very similar features. Our findings show that blink
ing interacts with the saccade premotor system already at the level of the
SC. The data also indicate that a neural mechanism, rather than passive ela
stic restoring forces within the oculomotor plant, underlies the compensati
on for blink-related perturbations. We propose that these interactions occu
r downstream from the motor SC and that the latter may encode the desired d
isplacement vector of the eyes by sending an approximately fixed number of
spikes to the brainstem saccadic burst generator.