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45 Cards in this Set

  • Front
  • Back
Smooth muscle
Skeletal / striated muscle
Cardiac muscle
Digestive system and other organs
Movement of body in relation to environment
Heart
Muscle inervation
One axon per muscle, but one m
Axon may innervate many muscle fibres, ex: eye 1:3 ratio, arm 1:100
Neuromuscular innervation
Axon releases acetylcholine, always excites, always contracts muscle. Muscle relaxes in absence of acetylcholine.
Antagonistic
Flexor
Extensor
Opposing sets of muscles
Brings hand to shoulder
Straightens out the arm
Red, pink, white fish muscles
Effect of cold water
Red: slow moevemtnts, don't fatigue
White: fast muscles, quick to fatigue
Pink are in the middle
-- cold water slows them down, but white muscles make up the difference in speed
Fast twitch
Slow twitch
Fast twitch are anaerobic, don't use glucose, fatigue quickly
- slow twitch are aerobic, use oxygen and glucose, don't tire quickly
Proprioceptor
Muscle proprioceptor
Receptor that detects the position /movement of a part of the body, ex the muscles.
- detects stretch, tell spinal cord /brain to contract it
Stretch reflex
Muscle spindle
Muscle Spindle proprioceptor responds to stretch: sensory nerve sends message to motor neuron in sp cord which sends message back to muscles around spindle, causes contraction. Neg fdbk loop
m spindle- proprioceptor that responds to stretch
Golgi tendon organs
Proprioceptors that respond to increase in muscle tension, located at tendons at opposite ends of muscle, they inhibit the motor neurons from contracting, put the brakes on the contraction
Reflex
Involuntary, automatic responses to stimuli. Ex clockwise foot and draw #6
Ballistic movement
A movement that can't be altered once it's been initiated ( like a thrown ball). Reflexes are ballistic, but there are feedback corrections that can correct them, thread needle- adjust thread
Central pattern generators
Neural mechanisms that generate rhythmic patterns of motor output. Ex wet dog shake. Cells In lumbar spine generate the rhythms even if they are severed from brain.
Babinsky reflex
Rooting reflex
Grasp reflex
Automatic reflexes
Touch bottom of baby foot, toes will spread
Touch cheek, mouth will open
Touch palm, fingers will grasp
Myasthenia gravis
Autoimune disease in which immune system forms antibodies that attack acetylcholine receptors at neuromuscular junctions--causes weakness and fatigue of skeletal muscles
Allied reflexes
More strong in infants and kids, one reflex initiates another. Ex, blow dust in face-- will close eyes then sneeze, leave dark movie theatre, see bright light you close eyes, then close mouth (maybe sneeze too)
Which area of the cerebral cortex controls motor mvmnt?
How? When?
Primary motor cortex (the pre central gyrus of the frontal cortex- just anterior to the central sulcus). How? Its axons extend to brainstem and sp cord, which in turn send impulses to muscles.
When: active when people INTEND a movement
--
Posterior parietal cortex
If damaged?
Keeps track of position of body relative to the world
-also important for planning movements.
- if damaged, they can describe what they see, but can't make action tword it (walk to, grasp, etc)
Premotor cortex
Prefrontal cortex
Active during preparations for movements, not so much during actual movements
- responds to light, noises and signals. Plans mvmnts according to probable outcomes (if damaged would shower w clothes on)
Supplimental motor cortex
Along w prefrontal cortex involved w planning rapid sequence movements (habitual mvmnts) that you do in certain order.
- supplementary inhibits the habit (ex: when you need to do something else)
Motor homunculus
The guy that is built to represent the percentages of body that relate to the primary motor cortex
Primary somatosensory cortex
Integrates touch information and movement
Brain mechanisms of:
- Prefrontal cortex
- Premotor cortex
- supplementary motor cortex
- responds to light, noise, sensory signals that lead to movement -- it calculates poss outcomes and plans mvmnt accordingly
- During preparation of mvmnt, gets info about the target and integrates body mvmnt and position in space
- organizes rapid sequence of mvmnt in partic order, acts just before the mvmnt occurs
Readiness potential
Which part of the brain is involved?
We become conscious of the decision to move after the process has already begun (approximate 500ms earlier in the flex wrist self report experiment.)
-the parietal cortex monitors the preparation of movement, including what we also feel as our "intention" to make the movement
Corrticospinal tracts
-two types
Paths from cerebral cortex to spinal cord
- lateral and medial corticospinal tracts
Lateral corticospinal tract
Set of axons that runs FROM primary motor cortex and the Red nucleus. Axons go down from cortex to target neurons in the sp cord.
In bulges in the medulla called pyramids, they cross over to the contralateral side and go to muscles that control the PERIPHERAL areas- hands and feet
Red nucleus
Midbrain area primarily responsible for controlling the arms. Lateral coticospinal tract axons extend from red nucleus to muscles on peripheral Areas
Medial corticospinal tract
Includes axons form many parts of cerebral cortex, as well as from midbrain tectum, reticular formation, vestibular nucleus. Axons on this tract go to both sides of the sp cord, controls trunk, neck shoulders, etc. Ie for walking. These movements /areas are bilateral, that's why tract doesn't just run down contralateral side.
How are touch receptors related to movement
Touch pathway goes from touch receptors to the brain, the corticospinal (lateral) tract goes from brain to medulla to spinal cord to muscles. You need to have touch in order to know where your hands and feet are in order to plan, make a mvmnt.
Paralysis
Lack of voluntary movement in part of the body

Due to damage in these cord, motor neurons, or axons
Parapalegia what and causes
Quadripilegia
P: loss of sensation and vol. Muscle control in both legs. Relfexes remain. Genitals: no messages to / brain but still respond to touch/orgasm.
Cause: cut through sp cord above segments attached to legs
Q: as above, but to all 4 extremities
Cause: cut in Sp cord above segments controlling arms
Hemipiligia what and cause
Loss of sensation & muscle control in arm& leg on one side.
Cause: damage to one hemisphere of cerebral cortex
Tabes dorsalis
Impaired sensation in legs & pelvic area. Impaired leg reflexes, walking, bladder & bowel control.
Causes: late stage syphilis, dorsal roots of sp cord deteriorate
Poliomyelitis
Paralysis
Causes: virus that damages cell bodies and motor neurons
Amyotrophic lateral sclerosis
Weakness then paralysis starts at arms then goes to legs. Motor neurons and axons from the brain to the (muscle?) are destroyed
AKA Lou Gherigs disease
Cause is unknown
Action potential in cerebellum
Action potential in the parallel fibers excite one purkinje cell after another. Purkinje cells send inhibitory message to cells in nuclei of cerebellum (which them send to midbrain and thalamus)
AP excites one purkinje cell the duration of the response. Cells arranged to precisely control the duration of outputs
Basal ganglia - Name parts
describe how chemical signal travels
Function of basal gangia
Group of subcortical structures in the forebrain (caudate nucleus, putamen, globus palliidus.
- Info fr: cerebral cortex to caudate and puatmen to globus pallidus to thalamus, to motor & prefrontal cortex.
- Releases GABA (inhibitory), selects and inhibits certain movements.
What happens to huntington's patients
Damage to basal ganglia means it is unable to inhibit unwanted behaviors, thus jerky extra movements of arms etc.
What kind of learning depends mostly on basal ganglia?
Motor habits that are difficult to describe in words (tie a necktie, drive a car, etc)
Difference btwn damage to spinal cord and damage to brain re: movement and other abilities
Damage to spinal cord results in loss of movement, but not cognitive loss or change, whereas damage to brain impairs movement as well as mood, memory and cognition.
Parkinsons disease
Symptoms
Rigidity of muscles, muscle tremors, slow movements. Toruble initiating physical and mental activity.
Get depressed, memory and reasoning deficits.
Parkinsons
Causes
Neurons in substantial nigra die off - they have dopamine releasing axons that go to caudate and putamen- less dopamine which means less excitation- which means less inhibition of globus- which means more inhibition of the thalamus - thus less excitation of cerebral cortex *** Net result: ultimately less stim of motor cortex, therefore slow movements ***
MPTP
L-dopa
Exposure to MPTP can induce parkinson's like symptoms
- L-dopa used in some cases to treat, it is precursor to dopamine and can cross blood brain barrier. But doesn't prevent neurons form dying, doesn't effectively replace dopamine, has nasty side effects
Other treatments for parkinson's
Electrical stimulation
Stem cells
To block tremor and enhance movement, but causes depression due to inhibition of seratonin
- stem cells can be used, or cells from aborted fetuses b/c they regrow to be healthy, still in early research stages with humans
Huntington's disease
Symptoms
Causes/hereditary
Jerk movements tremors, ultimately extensive brain damage.
CAG sequence -over 39 repetitions of CAG will be likely to get huntingdon's
Huntingtin
The gene responsible for huntington's disease alters the structure of s protien called huntingtin. The altered protein interferes with the functioning of the mitochondria