Chapter 8: Movement Flashcards
Muscles
Composed of fibers; each fiber is innervated by one motor neuron
Smooth muscle
internal organs, long, thin cells
Skeletal/striated muscle
main movers, long cylindrical fibers with stripes
cardiac muscle
heart; fused fibers contract together
Motor Unit
smallest functional unit
Neuron meets fiber at ?
Neuromuscular junction
Antagonistic muscles work in concert
Flexors vs Extensors
Myasthenia Gravis
autoimmune disorder; antibodies against ACh receptors
Symptoms of Myasthenia Gravis
progressive weakness, rapid fatigue of skeletal muscles
Physiological Basis of Myasthenia Gravis
fewer ACh receptors, morphological changes at synapse, action of Acetycholinsterase
Mammalian Muscles
Fast-twitch fibers and slow-twitch fibers
Fast-twitch fibers
contract and relax rapidly, anaerobic (no oxygen), fatigue rapidly, generate greatest force, (ex sprinting)
Slow-twitch fibers
longer contraction time, aerobic (oxygen), resistant to fatigue, generate much less force (walking)
Proprioceptors
Sensitive to position and movement of muscles; detect muscular stretch and tension; allows spinal cord to adjust signal
Two primary types of proprioceptors
Muscle spindles and golgi tendon organs
Muscle Spindles
parallel to muscle, senses stetch; muscle stretched -> signal motor neuron in spinal cord –> muscle contraction; negative feedback –> stretch causes contraction; stimulates Stretch reflex (knee-jerk)
Golgi Tendon organs
in tendons (connects muscles to bone), senses tension; vigorous muscle contraction –> signal spinal cord inhibitory interneurons –> inhibit motor neuron (inhibits contraction); negative feedback –> tension causes muscle relaxation; protects against vigorous contraction
Reflexes
consistent, automatic response to stimulu; allied reflexes occur together/ elicit each other
Ballistic movements
executed as a whole; cannot be corrected/not sensitive to feedback
Central Pattern Generators
neural mechanisms that generate rhythmic motor patters (wet dog shake, wing flapping in birds)
Major motor areas in FOREBRAIN
Cortex, basal ganglia
Major motor areas in MIDBRAIN
Substantia Nigra; Red Nucleus; Reticular Formation
Major motor areas in HINDBRAIN
Cerebellum, Reticular formation, vestibular nucleus
Primary Motor Cortex
coordinated movements in several muscles leading to specific outcome
Posterior Parietal Cortex
coordinating movement through environment based on visual input
prefrontal cortex
involved in planning movement
premotor cortex
involved in planning movement
supplementary cortex
involved in preparation for rapid sequences of movement
Dorsolateral Tract
carries axons from primary motor cortex and red nucleus to spinal interneurons controlling spinal motor neurons; THEN cross over to contralateral side at pyramids in ventral portion; THEN courses down dorsolateral portion of white matter of spinal cord; THEN controls movement of distal limbs (hands,fingers,toes)
Ventromedial Tract
Carries axons from primary motor cortex, axons from vestibular nucleus, tectum, reticular formation; THEN synapse on spinal interneurons controlling spinal motor neurons; THEN come axons cross, some dont, providing bilateral innervation; THEN courses down ventromedial portion of white matter of spinal cord; controls proximal limbs and axial musculature (neck, shoulders, trunk)
Motor functions of cerebellum
contains more neurons than rest of structures of brain combined; involved in: control of rapid eye movement, timing, establishment of new motor programs
Caudate Nucleus
primary input area; receives info from sensory areas of thalamus and cortex; receives important dopaminergic projection from substantia nigra in midbrain
putamen
same function
globus pallidus
primary output area; sends info to thalamus, which sends info to motor and prefrontal cortex, also midbrain
role of basal ganglia
organization of action sequences into chunks; inhibition of specific motor responses
Parkinson’s disease
degeneration of the dopaminergic neurons in the substantia nigra projecting to the caudate nucleus and putamen
symptoms of parkinson’s disease
rigidity; muscle tremors; slow movements; sometimes cognitive deficits; difficulty initiating movement; sometimes depression
frequency of parkinson’s disease
1/100 above age 50
Causes of Parkinson’s disease
early onset has genetic component; possible environmental influence
Treatment for Parkinson’s disease
L-dopa: crosses blood-brain barrier, where its absorbed by neurons and can increase dopamine production; cant restore degenerated neurons; effectiveness declines as disease progresses
Other possible treaments
Antioxidant drugs - decrease further damage; dopaminergic agonists - can cross blood-brain barrier; glutamate or adenosine antagonists; inactivating electrical stimulation of globus pallidus; neurotrophins - promote growth and survival of neurons; drugs that decrease apoptosis; fetal tissue transplants; drugs that block calcium channels abundant in elderly brains; drugs that stimulate cannabinoid receptors
