PY460: Biological Bases of BehaviorPY460: Biological Bases of BehaviorChapter 8: Movement

Module 8.1: The Control of MovementModule 8.2: Brain Mechanisms in MovementModule 8.3: 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 Muscles-- “The Final Path”- multiple fibers Smooth Muscle

movement of internal organs stomach, arterial lining

Cardiac muscles (myocardium)- interconnected bands of muscle

Skeletal Muscles- striated long cylindrical fibers- “striped appearance”

Slide 3: Muscle Movement: Axons and Acetylcholine

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

Neuromuscular junction- where the “motor neuron” meets a muscle fiber NTR of movement- acetylcholine effect: “contraction”, no Ach = relaxation

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

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

Proprioceptor: a receptor on the muscle sensitive to changes in muscle position and movement (“stretch”) of muscle. Respond with muscle contraction

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)

Life with reduced proprioception (babies, case in text)

Slide 6: Voluntary/Involutary Movements & Feedback

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

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

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

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)

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

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 Cortex- Adjacent Areas

Posterior Parietal Cortex- control actions related to visual or somatosensory stimuli. “cannot walk toward something they see”

Prefrontal Cortex- active in planning a potential movement- responds to sensory stimuli (future movement planning)

Premotor Cortex- active in preparation for movement, not during movement though.

Supplementary Motor Cortex- active during planning stage for rapid series of movements that require starting one movement before finishing another e.g., Typing

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

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 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

2 tracks act together to produce complete set of function muscle movements

Slide 13: The Cerebellum- “Follow My Finger”

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”

“Saccades”- ballistic eye movements from one fixation point to

another damage or drunkenness (cerebellum 1st place affected by

drink)- many small movements to fixate Finger-to-Nose- inaccurate first movement, finger wavers

during “hold”

Slide 14: Cellular Organization of Cerebellum& Duration of Movement

Perpendicular Organization of Cerebellar Cortex precisely organized cellular structure

Parallel Fibers Purkinge Cells (transmit to interior)

– fire separately– inhibitory

Duration of movement affected by number of Purkinge cells affected by

parallel fiber excitation

Slide 15: Basal Ganglia: Organizing Planned Movements

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 [video]

Symptoms- gradually increasing muscles tremors, slowed movement, inaccurate aim, difficult initiating physical, mental activity Muhammad Ali

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

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

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

Treatment: L-Dopa- cross BBB converted to dopamine. Stereotyped movements, Delusions, Hallucinations A “window” where helpful, soon disease too severe Nicotine-- Smoking??

Other Therapies [p.245]

Slide 18: Huntingdon’s Disease

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

Paralysis- Paraplegia- Quadriplegia- Poliomyelitis- Lou Gehrig’s Disease- Others

Flaccid Paralysis Spastic Paralysis Tabes Dorsalis