PY460: Biological Bases of Behavior
Chapter 8: Movement
Module 8.1:
Module 8.2:
Module 8.3:
The Control of Movement
Brain Mechanisms in Movement
Disorders of Movement
Slide 2: The Control of Movement
Introduction: Clip #10: Sensory Motor Integration
movement-- an extremely complex process
 complex “motor control” often w/o thought
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Muscles-- “The Final Path”- multiple fibers
Smooth Muscle
movement of internal organs
 stomach, arterial lining
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Cardiac muscles (myocardium) interconnected bands of muscle
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Skeletal Muscles- striated
long cylindrical fibers- “striped appearance”
Slide 3: Muscle Movement: Axons and Acetylcholine
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Axon to fiber ratio- greater the ratio the more precise
the movements [class; “typing with & w/o mittens]
 e.g., eye= 1:3 arm (bicep)
1:100
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Neuromuscular junction- where the “motor neuron”
meets a muscle fiber
NTR of movement- acetylcholine
effect: “contraction”, no Ach = relaxation
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Myasthenia Gravis- An “autoimmune disease”- body attacks
acetylcholine receptors
 2-3 per 100,000 over 75 years of age
 Symptoms-progressive weakening and rapid fatigue of striated
muscles as receptors are gradually destroyed.
 Treatment-Immune suppressants & drugs inhibiting
Acetylcholinesterase
Slide 4: Muscles Types and Functions
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Antagonistic Muscles- opposing sets of muscles
 Flexors- flexes or raises muscles
 Extensors- extends or straightens
Fish Muscles- (movements & duration)
 red (slow & long), pink (slow & not as long), white (fast & short)
Chicken Muscles (“white and dark meat”)
 breast- fast acceleration, short duration
 leg- long duration, not as fast (walking).
Human Muscles
 Fast Twitch (anaerobic)
– sprints/fast acceleration
 Slow Twitch (aerobic)
– duration/slow acceleration, speed
Slide 5: Proprioceptors-Feedback on Position & Movement
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Proprioceptor: a receptor on the muscle sensitive to changes in
muscle position and movement (“stretch”) of muscle. Respond
with muscle contraction
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Stretch Reflex- mediated at the spinal cord level
Muscle Spindle- stretch receptor attached parallel to
muscle fibers sensitive to elongation of fibers
knee-jerk response
Golgi Tendon Organ- responds to increases in muscle
tension.
 Prevents excessive vigorous contraction (which would
occur without it)
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Life with reduced proprioception (babies, case in text)
Slide 6: Voluntary/Involutary Movements & Feedback
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Types of Movements
Ballistic- large reflexive (all or none type) movements
Few ballistic movements-- most subject to feedback
modifications
Limits on Voluntary and Involuntary movement
few strictly involuntary, few strictly voluntary
limits of each (try swallowing 10 times)
Parkinson patients walking characteristics
INFANT REFLEXES: grasp reflex, Babinski reflex,
rooting reflex, allied reflex
presence in adults signal damage to Cerebral Cortex
Slide 7: Coordinated Movement
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Central Pattern Generator- proposed mechanism in
spinal cord or brain that generates rhythmic patterns of
“coordinated motor activity” that is extreme regular
within species
stimulation of this mechanism affect action, but not
frequency (apparently)
– dog shaking off water, scratching reflex
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Sequence of movements (e.g., walking) called a “Motor
Program”
 can be learned and built in. Think of a few!
 Can be part of evolutionary inheritance
– Yawning
Slide 8: The Spinal Cord-- Motor Program Keeper
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How is it that a chicken can run without its head?
In humans
chewing, swallowing, breathing are controlled below
the brain at the level of spinal cord/medulla.
Some motor programs (scratch reflex) are independent
of brain feedback altogether
isolating of “scratch reflex” neurons from brain axons
does not affect intrinsic firing rate and subsequent
behavior.
Rhythm of firing even unaffected by muscular
paralysis (the neurons are autorhythmic)
Slide 9: Brain and Movement (Begin Module 2)
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Areas to be discussed
Cortical Areas in Movement
 Primary Motor Cortex- messages (axons) to the medulla
and spinal cord (just anterior to the precentral gyrus of the
cerebral cortex)
– control of “complex movement plans”
– not reflexive (sneezing, cough, gag, cry etc.)
 Areas near Primary Motor Cortex
Medulla and Spinal Cord- receive messages from PMC,
control muscle movements (reflexive, bilateral, peripheral)
– not much in chap 8, but see table 8.1
Basal Ganglia & Cerebellum moderate movements but do
not directly cause. (“selection, order, smoothing & future
precision”)
Slide 10: The Cerebral Cortex
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Primary Motor Cortex
Fritsch & Hitzig- ESB of PMC= coordinated movement
No direct connections to muscles, rather controls
“complex movement plans” involving several
muscles, not individual muscles.
 i.e., activates central pattern generators
 see fig 8.9- “motor homunculus”
See Figure 8.10- distribution of cells activated
during hand movements
Slide 11: Working with the Primary Motor CortexAdjacent Areas
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Posterior Parietal Cortex- control actions related to visual or
somatosensory stimuli.
“cannot walk toward something they see”
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Prefrontal Cortex- active in planning a potential movementresponds to sensory stimuli (future movement planning)
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Premotor Cortex- active in preparation for movement, not
during movement though.
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Supplementary Motor Cortex- active during planning stage
for rapid series of movements that require starting one movement
before finishing another
e.g., Typing
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Preparation for Movement coordinated waves of activity among these structure sending
complex signals to PMC then down to the medulla and spinal cord.
Slide 12: Brain to Spinal Cord: 2 Tracks of Action
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Dorsolateral Tract- axons projecting from PMC and Red
Nucleus of Midbrain
axons cross over to opposite side of body controlling
peripheral unlearned fine movements.
 hands, fingers, toes
sometimes called the pyramidal tract
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Ventromedial Tract- axons from PMC and SMC
axons branch to both sides- damage affects coordinate
“side to side movements” like walking, standing, sitting,
“twisting”, that is “bilateral movements”.
 Neck, shoulders, trunk
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2 tracks act together to produce complete set of function
muscle movements
Slide 13: The Cerebellum- “Follow My Finger”
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Cerebellum- important in learned motor responses
programs allowing rapid sequential movement
damage-- trouble with rapid motor sequences requiring
accuracy and timing
 tapping to a rhythm
 speaking
 “adapting to prisms that distort vision”
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“Saccades”- ballistic eye movements from one fixation point to
another
damage or drunkenness (cerebellum 1st place affected by
drink)- many small movements to fixate
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Finger-to-Nose- inaccurate first movement, finger wavers
during “hold”
Slide 14: Cellular Organization of Cerebellum
& Duration of Movement
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Perpendicular Organization of Cerebellar Cortex
precisely organized cellular structure
 Parallel Fibers
 Purkinge Cells (transmit to interior)
– fire separately
– inhibitory
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Duration of movement
affected by number of Purkinge cells affected by
parallel fiber excitation
Slide 15: Basal Ganglia: Organizing Planned Movements
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Basal Ganglia has many roles- damage often results in
much more than movement problems (e.g., memory,
problem solving).
but some insight on its contributions to movement
 seems to help in organizing new and habitual movements
and inhibit unwanted movements (caudate nucleus)
– e.g., signing your name
 study of clumsy children
Slide 16: Parkinson’s Disease
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[video]
Symptoms- gradually increasing muscles tremors, slowed
movement, inaccurate aim, difficult initiating physical, mental
activity
Muhammad Ali
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Prevalence: 1 per 100 over age 50
Physiology- cell degradation in the substantia nigra & amygdala
decreased dopamine at D1 and D2 receptors resulting in net inhibitory
response, thus “downstream” decreased excitation by cerebral cortex
and thalamus
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Natural degradation with age, some start with less cells, or lose at
faster rate than others.
[Early and Late-Onset Parkinson’s (p.243)]
Slide 17: Etiology and Treatment of Parkinson’s
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Suggested Causes
 Inheritance
Interrupted blood flow to areas of the brain
Previous encephalitis or viral infection
Prolonged exposure to drugs/toxins
 unlikely however that cause of most cases are due to drug abuse or
exposure to toxin (Paraquat) (MPP+ MPTP).
– Likely these factors contribute to process of degradation already active
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Treatment: L-Dopa- cross BBB converted to dopamine.
Stereotyped movements, Delusions, Hallucinations
A “window” where helpful, soon disease too severe
Nicotine-- Smoking??
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Other Therapies [p.245]
Slide 18: Huntingdon’s Disease
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A severe neurological disorder marked by gradually
worsening tremors/twitches to severe writhing affecting
daily movements like talking, walking, eating etc.
Prevalence: 1 per 10,000
Widespread brain damage, particular area releasing
GABA an inhibitory neurotransmitter
especially in basal ganglia (caudate nucleus etc.)
Genetic Conditions/Considerations
A dominant mutant gene.. Thus parent has 50% chance of
passing disorder on.
Can test for the gene to determine not only who will get, but
approximately when.
In vitro testing, other ethical issues
Slide 20: Spinal Cord Disorders
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ParalysisParaplegiaQuadriplegiaPoliomyelitisLou Gehrig’s DiseaseOthers
Flaccid Paralysis
Spastic Paralysis
Tabes Dorsalis