Biomedical Engineering Reference
In-Depth Information
The FN receives input from the SC, as well as other sites. The output of the FN is
excitatory and projects ipsilaterally and contralaterally, as shown in Figure 13.58. During
fixation, the FN fires tonically at low rates. Twenty ms prior to a saccade, the contralateral
FN bursts, and the ipsilateral FN pauses and then discharges with a burst. The pause in
ipsilateral firing is due to Purkinje cell input to the FN. The sequential organization of
Purkinje cells along beams of parallel fibers suggests that the cerebellar cortex might func-
tion as a delay, producing a set of timed pulses that could be used to program the duration
of the saccade. If one considers nonprimary position saccades, different temporal and
spatial schemes, via cerebellar control, are necessary to produce the same-size saccade.
It is postulated here that the cerebellum acts as a gating device that precisely terminates a
saccade based on the initial position of the eye in the orbit.
To execute a saccade, a sequence of complex activities takes place within the brain,
beginning from the detection of an error on the retina to the actual movement of the eyes.
A saccade is directly caused by a burst discharge (pulse) from motoneurons stimulating
the agonist muscle and a pause in firing from motoneurons stimulating the antagonist
muscle. During periods of fixation, the motoneurons fire at a rate necessary to keep the
eye stable (step). The pulse discharge in the motoneurons is caused by the EBN, and the
step discharge is caused by the TN in the PPRF.
Consider the saccade network in Figure 13.57 that is programmed to move the eyes 20 .
Qualitatively, a saccade occurs according to the following sequence of events:
1. The deep layers of the SC initiate a saccade based on the distance between the current
position of the eye and the desired target. The neural activity in the SC is organized
into movement fields that are associated with the direction and saccade amplitude, and it
does not involve the initial position of the eyeball whatsoever. Neurons active in the SC
during this particular saccade are shown as the dark circle, representing the desired 20
eye movement. Active neurons in the deep layers of the SC generate an irregular high-
frequency burst of activity that changes over time, beginning 18-20 ms before a saccade
and ending sometime toward the end of the saccade; the exact timing for the end of the
SC firing is quite random and can occur either before or after the saccade ends.
2. The ipsilateral LLBN and EBN are stimulated by the contralateral SC burst cells. The
LLBN then inhibits the tonic firing of the OPN. The contralateral FN also stimulates
the ipsilateral LLBN and EBN.
3. When the OPN cease firing, the MLBN (EBN and IBN) is released from inhibition. Some
report that the ipsilateral EBN is probably not stimulated by the SC [25, 39]. This conflict
doesn't impact our model as we propose the stimulation of the EBN by other sites does
not reflect the firing rate of the EBN, but that the EBN fire autonomously given weak
stimulation.
4. The ipsilateral IBN is stimulated by the ipsilateral LLBN and the contralateral FN of the
cerebellum. When released from inhibition, the ipsilateral EBN responds with a PIRB for
a brief period of time. The EBN when stimulated by the contralateral FN (and perhaps
the SC) enables a special membrane property that causes a high-frequency burst that
decays slowly until inhibited by the contralateral IBN. The IBN may also have the same
type of special membrane properties.
5. The burst firing in the ipsilateral IBN inhibits the contralateral EBN and Abducens
Nucleus, and the ipsilateral Oculomotor Nucleus.
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