Odds and ends:
motor cortex
basal ganglia Kandel et al Ch 43
eye movements Kandel et al Ch 44
Coding in Motor Cortex (ctd)
Graziano et al, 2002: prolonged electircal stimulation (500 msec) leads to adoption of
particular postures. Lines show arm trajectory from random starting point
Other cells: movement amplitude, direction, speed
But note other findings that M1 cells code force
Consequences of cerebellar damage:
Flaccidity in primates, rigidity in cats - Consequence of changes in
sensitivity of spinal reflex circuits.
Ataxia = lack of coordination
Disarthria = slurred speech
Nystagmus = eye drift followed by rapid corrections
Hypermetria = overshoot when pointing to a target
Intention tremor = oscillating limb when pointing
Unilateral cerebellar damage: subjects alternates palm up – palm down
Similar effects of alcohol
Different regions of the cerebellum involved in different aspects of motor control.
Laetral regions active before movement.
Medial regions active during movement.
The relationships of the basal ganglia to the major components of the motor system. The basal ganglia and
cerebellum may be viewed as key elements in two parallel reentrant systems that receive input from and
return their influences to the cerebral cortex through discrete and separate portions of the ventrolateral
thalamus. They also influence the brain stem and, ultimately, spinal mechanisms.
The four principal nuclei of the basal ganglia are (1) the striatum, (2) the globus pallidus (or pallidum),
(3) the substantia nigra (consisting of the pars reticulata and pars compacta), and (4) the subthalamic
nucleus. The striatum consists of three important subdivisions: the caudate nucleus, the putamen, and the
ventral striatum (which includes the nucleus accumbens). The striatum is divided into the caudate nucleus
and putamen by the internal capsule, a major collection of fibers that run between the neocortex and thalamu
in both directions.
Striatum = caudate+putamen
The striatum receives input from nearly all the
cerebral cortex. Functionally related cortical areas
project to overlapping striatal zones and an individual
cortical area projects to several striatal zones. Cortical areas
not functionally related project to separate
zones of the striatum, although there may be
some interaction between adjacent zones.
2. The striatum sends a focused and convergent
inhibitory projection to the basal ganglia output
nuclei, GPi and SNpr.
3. The STN receives input from the frontal lobe,
especially from the motor, premotor, and
supplementary motor cortex and from the frontal
eye fields.
4. The STN sends a fast divergent excitatory
projection to GPi and SNpr.
5. Reciprocal and loop-like connection
among basal ganglia nuclei that may play a
negative or positive feedback role or may result in
focusing of signals.
6. The output from the basal ganglia (GPi and SNpr)
is inhibitory and projects to motor areas in the
brain stem and thalamus.
7. There are no direct connections between the
basal ganglia and the spinal sensory or motor
Changes in the activity of basal ganglia occur at
the onset of movement but after the muscles are
already active. Thus, they are unlikely to initiate
The striatum is the major recipient of inputs to the basal
ganglia from the cerebral cortex, thalamus, and brain stem.
Its neurons project to the globus pallidus and substantia nigra.
These two nuclei, give rise to the major output
projections from the basal ganglia.
The anatomic connections of the basal
ganglia-thalamocortical circuitry, indicating the parallel
direct and indirect pathways from the striatum to the basal
ganglia output nuclei. Two types of dopamine receptors
(D1 and D2) are located on different sets of output neurons
in the striatum that give rise to the direct and indirect
Pink =excitatory
Gray= inhibitory
The frontal lobe targets of the basal ganglia-thalamocortical circuits.
ACA = anterior cingulate area; FEF = frontal eye field; MOFC = medial orbitofrontal
cortex; PMC = premotor cortex; SEF = supplementary eye field; SMA = supplementary motor area.
dorsolateral prefrontal ctx
lateral orbitofrontal ctx
primary motor crtx
Hypokinetic disorders (eg Parkinson disease) characterized
by impaired initiation of movement (akinesia) and
reduced amplitude and velocity of voluntary movement
(bradykinesia). Usually accompanied by rigidity) and
Hyperkinetic disorders (Huntington disease and
hemiballismus) characterized by excessive motor
activit, - involuntary movements (dyskinesias) and
decreased muscle tone (hypotonia). The involuntary
movements may be slow, writhing movements of the
extremities (athetosis); jerky, random movements of
the limbs and orofacial structures (chorea);
violent, large-amplitude, proximal limb movements
(ballism), and more sustained abnormal postures and
slower movements with underlying
cocontraction of agonist and antagonist muscles
Darker arrows increased activity
Lighter arrows decreased activity
Neurons in substantia nigra pc in basal ganglia release dopamine.
These neurons signal expected reward.
Cells do not discharge during movement.
SNpc likely to play a critical role in some types of motor learning.
Dopaminergic neurons in basal ganglia signal expected reward.
(Schultz, 2000)
Response to unexpected
Increased firing for earlier or
later reward
Expected reward is
Hypotheses about basal ganglia function:
1. basal ganglia do not initiate movement, they contribute to the automatic
execution of movement sequences. Other mechanisms initiate the first component
in a sequence, but that basal ganglia contain the programs for completion of
the sequence.
2. the basal ganglia circuitry is made up of opposing parallel pathways that
adjust the magnitude of the inhibitory GPi output in order to increase or
decrease movement. Increased GPi output slows movements
and decreased GPi output increases movement.
3. basal ganglia act to permit desired movements and to inhibit unwanted
competing movements.
Why do we move our eyes?
- Image stabilization
- Information acquisition
Visual Acuity matches photoreceptor density
Why do we move our eyes?
1. To bring objects of interest onto high acuity region in fovea.
Cone Photoreceptors are densely packed in the central fovea
Why eye movements are hard to measure.
A small eye rotation translates into a big change in visual angle
Visual Angle
tan(a/2) = x/d
a = 2 tan 1 x/d
1 diopter = 1/focal length in meters
0.3mm = 1 deg visual angle
55 diopters = 1/.018
Why do we move our eyes?
1. To bring objects of interest onto high acuity region in fovea.
2. Cortical magnification suggests enhanced processing of image
in the central visual field.
Oculomotor Muscles
Muscles innervated by oculomotor, trochlear, and abducens (cranial) nerves from the
oculomotor nuclei in the brainstem. Oculo-motor neurons: 100-600Hz vs spinal motor
Neurons: 50-100Hz
Types of Eye Movement
Information Gathering
Voluntary (attention)
vestibular ocular reflex (vor)
new location, high velocity (700 deg/sec),
body movements
Smooth pursuit
optokinetic nystagmus (okn)
object moves, velocity, slow(ish)
whole field image motion
change point of fixation in depth
slow, disjunctive (eyes rotate in opposite directions)
(all others are conjunctive)
Note: link between accommodation and vergence
Fixation: period when eye is relatively stationary between saccades.
Retinal structure
Accomodation:tension on zonule fibres
Latency of vestibular-ocular reflex=17msec
“main sequence”: duration = c Amplitude + b
Min saccade duration approx 25 msec, max approx 200msec
Demonstration of “miniature” eye movements
It is almost impossible to hold the eyes still.
What’s involved in making a saccadic eye movement?
Behavioral goal: make a sandwich
Sub-goal: get peanut butter
Visual search for pb: requires memory for eg color of pb or location
Visual search provides saccade goal - attend to target location
Plan saccade to location (sensory-motor transformation)
Coordinate with hands/head
Calculate velocity/position signal
Execute saccade/
Brain Circuitry for Saccades
1. Neural activity
related to saccade
2. Microstimulation
generates saccade
3. Lesions impair
V1: striate cortex
Basal ganglia
Oculomotor nuclei
Function of Different Areas
target selection
saccade decision
saccade command
inhibits SC
(where to go)
signals to muscles
Posterior Parietal Cortex
Intra-Parietal Sulcus: area
of multi-sensory convergence
LIP: Lateral Intra-parietal Area
Target selection for saccades: cells fire before saccade to attended object
Frontal eye fields
Voluntary control
of saccades.
Selection from
multiple targets
Relates to
behavioral goals.
Supplementary eye fields
-Planning/ Error
-relates to behavioral
Pre-motor neurons
Motor neurons
Motor neurons for the eye muscles are located in the oculomotor nucleus (III), trochlear nucleus (IV), and
abducens nucleus (VI), and reach the extraocular muscles via the corresponding nerves (n. III, n. IV, n. VI).
Premotor neurons for controlling eye movements are located in the paramedian pontine reticular formation
(PPRF), the mesencephalic reticular formation (MRF), rostral interstitial nucleus of the medial longitudinal
fasciculus (riMLF), the interstitial nucleus of Cajal (IC), the vestibular nuclei (VN), and the nucleus
prepositus hypoglossi (NPH).
Brain areas involved in making a saccadic eye movement
Behavioral goal: make a sandwich (learn how to make sandwiches)
Frontal cortex.
Sub-goal: get peanut butter (secondary reward signal - dopamine - basal
Visual search for pb: requires memory for eg color of pb or location
(memory for visual properties - Inferotemporal cortex; activation of
color - V1, V4)
Visual search provides saccade goal. LIP - target selection, also FEF
Plan saccade - FEF, SEF
Coordinate with hands/head
Execute saccade/ control time of execution: basal ganglia (substantia
nigra pars reticulata, caudate)
Calculate velocity/position signal oculomotor nuclei
Relation between saccades and attention.
Saccade is always preceded by an attentional shift
However, attention can be allocated covertly to the
peripheral retina without a saccade.
Pursuit movements also require attention.
Superior colliculus
Brain Circuitry for Pursuit
& Supplementary
Smooth pursuit
Velocity signal
Early motion analysis
RF reticular formation
VN vestibular nucle
PN , pontine nucleii
OV oculomotor vermis
VPF ventral paraflocculus
FN fastigial nucleus
Visual Stability

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